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細川義隆

徳島大学

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Jグローバル
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2024年5月3日更新

職名: 講師
電話: 633-7340
電子メール: hosokawa@tokushima-u.ac.jp
学歴: 1997/3: 徳島大学歯学部歯学科卒業
2001/3: 徳島大学大学院歯学研究科博士課程修了
学位: 博士(歯学) (徳島大学) (2001年3月)
職歴・経歴: 2001/4: 徳島大学歯学部附属病院，研修医
2002/2: Postdoctoral Fellow, The Forsyth Institute, Department of Immunology
2002/4: 徳島大学歯学部歯学科，歯科保存学第一講座，助手
2004/4: 徳島大学大学院ヘルスバイオサイエンス研究部，発達予防医歯学部門，健康長寿歯科学講座，助手
2004/6: 徳島大学·医学部歯学部附属病院，診療科，歯科，助手

専門分野・研究分野: 歯周炎

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2024年5月3日更新

専門分野・研究分野: 歯周炎
担当経験のある授業科目: 保存修復学各論 (学部)
保存修復学実習 (学部)
保存修復学総論 (学部)
再生歯科治療学 (大学院)
口腔機能再建学実験実習 (大学院)
実践口腔科学実習 (大学院)
歯内治療学 (学部)
歯内治療学1 (学部)
歯科保存学(1) 実習 (学部)
歯科保存学(1)B 講義 (学部)
歯科臨床示説 (学部)
指導経験: 1人 (博士)

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2024年5月3日更新

専門分野・研究分野: 歯周炎

研究テーマ: 歯周炎病変局所へのリンパ球浸潤機構に関する研究 (歯周炎 (periodontal disease))

著書

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論文

Risa Okamoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Keiichi Hosaka :
Cardamonin decreases inflammatory mediator expression in IL-1β-stimulated human periodontal ligament cells.,
Molecular Biology Reports, Vol.51, No.1, 2024.

(要約): In this study, we found that cardamonin could suppress the production of inflammatory mediators in HPDLCs as well as the activation of several signaling pathways induced by IL-1β treatment.
(キーワード): Chalcones / Interleukin-1beta / Periodontal Ligament / NF-kappa B / Cytokines / Cyclooxygenase 2 / Chemokines / Inflammation Mediators
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s11033-023-09204-8
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38281189; ● Search Scopus @ Elsevier (PMID): 38281189; ● Search Scopus @ Elsevier (DOI): 10.1007/s11033-023-09204-8

(DOI: 10.1007/s11033-023-09204-8, PubMed: 38281189) Yoshitaka Hosokawa, Ikuko Hosokawa, Masahiro Shimoyama, Risa Okamoto, Kazumi Ozaki and Keiichi Hosaka :
The effects of berteroin on inflammatory mediators and antioxidant enzymes expression in human periodontal ligament cells.,
Naunyn-Schmiedeberg's Archives of Pharmacology, 2023.

(要約): Berteroin is a bioactive substance classified as an isothiocyanate found in cruciferous vegetables such as cabbage, arugula, and salad leaves. In this study, we aimed to determine whether berteroin exerts anti-inflammatory effects on human periodontal ligament cells (HPDLCs), a resident cells of periodontal tissue. Berteroin suppressed interleukin (IL)-1β or tumor necrosis factor (TNF)-α-induced chemokines (C-C motif chemokine ligand (CCL)2, CCL20, C-X-C motif chemokine ligand (CXCL)10, IL-8, and IL-6) production and intercellular adhesion molecule (ICAM)-1 expression in HPDLCs. In addition, berteroin inhibited phosphorylation of IκB kinase (IKK)- α/ β, nuclear factor (NF)- κB p65, and IκB- α and degradation of IκB- α in the NF-κB pathway induced by IL-1 β or TNF- α stimulation. Moreover, berteroin could inhibit signal transducer and activator of transcription (STAT)3 phosphorylation in TNF- α -stimulated HPDLC. Furthermore, berteroin increased the expression of the antioxidant enzymes, heme oxygenase (HO)-1 and NAD(P)H quinone dehydrogenase (NQO)1, in IL-1 β or TNF- α -stimulated HPDLCs. These results suggest that berteroin may decrease the production of inflammatory mediators in HPDLCs by suppressing the NF-κB pathway, and may also decrease the local reactive oxygen species (ROS) production in periodontal lesions by increasing the production of antioxidant enzymes.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s00210-023-02761-6
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37804343; ● Search Scopus @ Elsevier (PMID): 37804343; ● Search Scopus @ Elsevier (DOI): 10.1007/s00210-023-02761-6

(DOI: 10.1007/s00210-023-02761-6, PubMed: 37804343) Masahiro Shimoyama, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Keiichi Hosaka :
Effects of erucin on inflammatory mediators and antioxidant enzymes' expression in TNF-α-stimulated human oral epithelial cells.,
Immunopharmacology and Immunotoxicology, Vol.46, No.1, 49-54, 2023.

(要約): These results suggest that erucin may provide a new anti-inflammatory agent that can be used in the treatment of periodontitis.
(キーワード): Humans / Tumor Necrosis Factor-alpha / Antioxidants / Inflammation Mediators / Epithelial Cells / NF-kappa B / Chemokines / Periodontitis / Sulfides / Thiocyanates
(出版サイトへのリンク): ● Publication site (DOI): 10.1080/08923973.2023.2250551
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37624680; ● Search Scopus @ Elsevier (PMID): 37624680; ● Search Scopus @ Elsevier (DOI): 10.1080/08923973.2023.2250551

(DOI: 10.1080/08923973.2023.2250551, PubMed: 37624680) Yoshitaka Hosokawa, Ikuko Hosokawa, Masahiro Shimoyama, Ayumi Fujii, Juri Sato, Kimitake Kadena, Kazumi Ozaki and Keiichi Hosaka :
The Anti-Inflammatory Effects of Iberin on TNF-α-Stimulated Human Oral Epithelial Cells: In Vitro Research.,
Biomedicines, Vol.10, No.12, 2022.

(要約): Iberin is a bioactive chemical found in cruciferous plants that has been demonstrated to have anticancer properties. However, there have been no reports on its effects on periodontal resident cells, and many questions remain unanswered. The aim of this study was to examine whether iberin had anti-inflammatory effects on human oral epithelial cells, including influences on signal transduction pathway activation in TNF-α-στιμυλατεd χελλσ. Iberin inhibited the production of interleukin (IL)-6 and C-X-C motif chemokine ligand 10 (CXCL10), as well as the expression of vascular cell adhesion molecule (VCAM)-1, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2 in tumor necrosis factor (TNF)-α-stimulated TR146 cells, a human oral epithelial cell line. Moreover, iberin administration increased the expression of antioxidant signaling pathways, such as Heme Oxygenase (HO)-1 and NAD(P)H quinone dehydrogenase 1 (NQO1). Furthermore, we found that iberin could inhibit the activation of the nuclear factor (NF)-κB, signal transducer and activator of transcription (STAT)3, and p70S6 kinase (p70S6K)-S6 ribosomal protein (S6) pathways in TNF-α-stimulated TR146 cells. In conclusion, iberin reduced inflammatory mediator expression in human oral epithelial cells by preventing the activation of particular signal transduction pathways.
(徳島大学機関リポジトリ): ● Metadata: 118001
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/biomedicines10123155
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36551911; ● Search Scopus @ Elsevier (PMID): 36551911; ● Search Scopus @ Elsevier (DOI): 10.3390/biomedicines10123155

(徳島大学機関リポジトリ: 118001, DOI: 10.3390/biomedicines10123155, PubMed: 36551911) Masahiro Shimoyama, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Keiichi Hosaka :
6-(Methylsulfinyl) Hexyl Isothiocyanate Inhibits IL-6 and CXCL10 Production in TNF-α-Stimulated Human Oral Epithelial Cells.,
Current Issues in Molecular Biology, Vol.44, No.7, 2915-2922, 2022.

(要約): 6-(Methylsulfinyl) hexyl isothiocyanate (6-MSITC) is a bioactive substance found in wasabi (Wasabia japonica) and has been reported to have some bioactive effects including anticancer and antioxidant effects. However, there are no reports on its effects on periodontal resident cells, and many points remain unclear. In this study, we aimed to investigate whether 6-MSITC exerts anti-inflammatory effects on human oral epithelial cells, including effects on signal transduction pathway activation. 6-MSITC inhibited interleukin (IL)-6 and C-X-C motif chemokine ligand 10 (CXCL10) production in TNF-α-stimulated TR146 cells, which are a human oral epithelial cell line. Moreover, we found that 6-MSITC could suppress signal transducer and activator of transcription (STAT)3, nuclear factor (NF)-κB, and p70S6 kinase (p70S6K)-S6 ribosomal protein (S6) pathways activation in TNF-α-stimulated TR146 cells. Furthermore, STAT3 and NF-κB inhibitors could suppress IL-6 and CXCL10 production in TNF-α-treated TR146 cells. In summary, 6-MSITC could decrease IL-6 and CXCL10 production in human oral epithelial cell by inhibiting STAT3 and NF-κB activation.
(徳島大学機関リポジトリ): ● Metadata: 117734
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/cimb44070201
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35877425; ● Search Scopus @ Elsevier (PMID): 35877425; ● Search Scopus @ Elsevier (DOI): 10.3390/cimb44070201

(徳島大学機関リポジトリ: 117734, DOI: 10.3390/cimb44070201, PubMed: 35877425) Yoshitaka Hosokawa, Ikuko Hosokawa and Kazumi Ozaki :
Nobiletin Decreases Inflammatory Mediator Expression in Tumor Necrosis Factor-Stimulated Human Periodontal Ligament Cells.,
Mediators of Inflammation, Vol.2021, No.5535844, 2021.

(要約): B and AKT1 activations and upregulating the NFE2L2 and HMOX1 expression.
(徳島大学機関リポジトリ): ● Metadata: 116565
(出版サイトへのリンク): ● Publication site (DOI): 10.1155/2021/5535844
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34335088; ● Search Scopus @ Elsevier (PMID): 34335088; ● Search Scopus @ Elsevier (DOI): 10.1155/2021/5535844

(徳島大学機関リポジトリ: 116565, DOI: 10.1155/2021/5535844, PubMed: 34335088) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
Nobiletin Inhibits Inflammatory Reaction in Interleukin-1β-Stimulated Human Periodontal Ligament Cells.,
Pharmaceutics, Vol.13, No.5, 667, 2021.

(要約): The immune response in periodontal lesions is involved in the progression of periodontal disease. Therefore, it is important to find a bioactive substance that has anti-inflammatory effects in periodontal lesions. This study aimed to examine if nobiletin, which is found in the peel of citrus fruits, could inhibit inflammatory responses in interleukin (IL)-1β-stimulated human periodontal ligament cells (HPDLCs). The release of cytokines (IL-6, IL-8, CXCL10, CCL20, and CCL2) and matrix metalloproteinases (MMP-1 and MMP-3) was assessed by ELISA. The expression of cell adhesion molecules (ICAM-1and VCAM-1) and the activation of signal transduction pathways (nuclear factor (NF)-κB, mitogen-activated protein kinases (MAPKs) and protein kinase B (Akt)) in HPDLCs were detected by Western blot analysis. Our experiments revealed that nobiletin decreased the expression of inflammatory cytokines, cell adhesion molecules, and MMPs in IL-1β-stimulated HPDLCs. Moreover, we revealed that nobiletin treatment could suppress the activation of the NF-κB, MAPKs, and Akt pathways. These findings indicate that nobiletin could inhibit inflammatory reactions in IL-1β-stimulated HPDLCs by inhibiting multiple signal transduction pathways, including NF-κB, MAPKs, and Akt.
(徳島大学機関リポジトリ): ● Metadata: 116619
(出版サイトへのリンク): ● Publication site (DOI): 10.3390/pharmaceutics13050667
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34066937; ● Search Scopus @ Elsevier (PMID): 34066937; ● Search Scopus @ Elsevier (DOI): 10.3390/pharmaceutics13050667

(徳島大学機関リポジトリ: 116619, DOI: 10.3390/pharmaceutics13050667, PubMed: 34066937) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
The Polymethoxy Flavonoid Sudachitin Inhibits Interleukin-1 β-Induced Inflammatory Mediator Production in Human Periodontal Ligament Cells,
BioMed Research International, Vol.2021, No.Article ID 8826586, 2021.

(徳島大学機関リポジトリ): ● Metadata: 116275
(出版サイトへのリンク): ● Publication site (DOI): 10.1155/2021/8826586
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 33575345; ● Search Scopus @ Elsevier (PMID): 33575345; ● Search Scopus @ Elsevier (DOI): 10.1155/2021/8826586

(徳島大学機関リポジトリ: 116275, DOI: 10.1155/2021/8826586, PubMed: 33575345) Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki and Takashi Matsuo :
Carnosic acid inhibits inflammatory cytokines production in human periodontal ligament cells.,
Immunopharmacology and Immunotoxicology, Vol.42, No.4, 373-378, 2020.

(要約): The results of this study suggest that CA has anti-inflammatory effects in human periodontal ligament cells by inhibiting JNK, NF-κB and STAT3 pathways.
(出版サイトへのリンク): ● Publication site (DOI): 10.1080/08923973.2020.1782427
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32538208; ● Summary page in Scopus @ Elsevier: 2-s2.0-85087515653

(DOI: 10.1080/08923973.2020.1782427, PubMed: 32538208, Elsevier: Scopus) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
Sudachitin Inhibits Matrix Metalloproteinase-1 and -3 Production in Tumor Necrosis Factor-α-Stimulated Human Periodontal Ligament Cells.,
Inflammation, Vol.42, No.4, 1456-1462, 2019.

(要約): Sudachitin, a polymethoxylated flavonoid found in the skin of Citrus sudachi, is a biologically active substance. The aim of this study was to examine whether sudachitin could be used to inhibit the expression of matrix metalloproteinase (MMP)-1 and MMP-3, which are involved in the destruction of periodontal tissues in periodontal lesions, in tumor necrosis factor (TNF)-α-stimulated human periodontal ligament cells (HPDLC). Sudachitin suppressed TNF-α-induced MMP-1 and MMP-3 production in HPDLC. On the other hand, it enhanced tissue inhibitor of metalloproteinase (TIMP)-1 expression. The level of Akt phosphorylation in the TNF-α-stimulated HPDLC was decreased by sudachitin treatment. Moreover, an Akt inhibitor reduced MMP-1 and MMP-3 production and increased TIMP-1 production. These findings indicate that sudachitin reduces MMP-1 and MMP-3 production in TNF-α-stimulated HPDLC by inhibiting the Akt pathway.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10753-019-01007-z
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30997585; ● Search Scopus @ Elsevier (PMID): 30997585; ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-019-01007-z

(DOI: 10.1007/s10753-019-01007-z, PubMed: 30997585) Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki and Takashi Matsuo :
Carnosic Acid Inhibits CXCR3 Ligands Production in IL-27-Stimulated Human Oral Epithelial Cells.,
Inflammation, Vol.42, No.4, 1311-1316, 2019.

(要約): Carnosic acid, which is a bioactive compound isolated from rosemary, has various pharmacological effects. However, the anti-inflammatory effect of carnosic acid on periodontitis is still unknown. The aim of this study was to investigate the effect of carnosic acid on CXC chemokine receptor 3 (CXCR3) ligands, which are involved in Th1 cells migration and accumulation, production in interleukin (IL)-27-stimulated human oral epithelial cells (TR146 cells). Carnosic acid decreased CXC chemokine ligand (CXCL)9, CXCL10, and CXCL11 production in IL-27-stimulated TR146 cells in a dose-dependent fashion. Moreover, we disclosed that carnosic acid could suppress signal transducer and activator of transcription (STAT)1, STAT3, and protein kinase B (Akt) phosphorylation in IL-27-stimulated TR146 cells. Furthermore, STAT1, STAT3, and Akt inhibitors could suppress CXCR3 ligands production in IL-27-treated TR146 cells. In summary, carnosic acid could reduce CXCR3 ligands production in human oral epithelial cell by inhibiting STAT1, STAT3, and Akt activation.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10753-019-00991-6
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30820808; ● Search Scopus @ Elsevier (PMID): 30820808; ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-019-00991-6

(DOI: 10.1007/s10753-019-00991-6, PubMed: 30820808) Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa and Hideki Shiba :
Interleukin (IL)-35 Suppresses IL-6 and IL-8 Production in IL-17A-Stimulated Human Periodontal Ligament Cells.,
Inflammation, Vol.42, No.3, 835-840, 2019.

(要約): Interleukin (IL)-35 is a novel anti-inflammatory cytokine that is produced by regulatory T cells. IL-35 is reported to suppress IL-17A-producing helper T (Th17) cell activation. IL-17A is related to progression of periodontitis. Furthermore, IL-35 and IL-17A are detected in human gingival crevicular fluid. However, the effect of IL-35 and interaction between IL-35 and IL-17A on pro-inflammatory cytokine production in human periodontal resident cells are still unclear. The aim of this study was to clarify the effect of IL-35 on IL-6 and IL-8 production in human periodontal ligament cells (HPDLCs) stimulated with IL-17A. IL-35 inhibited IL-6 and IL-8 production in IL-17A-stimulated HPDLCs. Moreover, western blot analysis showed that IL-35 suppressed extracellular signal-regulated kinase (ERK) and nuclear factor (NF)-κB p65 phosphorylation in IL-17A-stimulated HPDLCs. Our findings suggested that IL-35 produced from regulatory T cells might inhibit progression of periodontitis by decreasing IL-17A-induced levels of IL-6 and IL-8.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10753-018-0938-9
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30484005; ● Search Scopus @ Elsevier (PMID): 30484005; ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-018-0938-9

(DOI: 10.1007/s10753-018-0938-9, PubMed: 30484005) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
Honokiol and Magnolol Inhibit CXCL10 and CXCL11 Production in IL-27-Stimulated Human Oral Epithelial Cells.,
Inflammation, Vol.41, No.6, 2110-2115, 2018.

(要約): Honokiol and magnolol, which are lignans isolated from Magnolia quinquepeta, have some pharmacological effects. However, the anti-inflammatory effects of honokiol and magnolol on periodontal disease are still uncertain. The aim of this study was to examine the effect of honokiol and magnolol on CXC chemokine receptor 3 (CXCR3) ligands, which are related with Th1 cell migration, production in interleukin (IL)-27-stimulated human oral epithelial cells (TR146 cells). Honokiol and magnolol inhibited CXC chemokine ligand (CXCL)10 and CXCL11 production in IL-27-stimulated TR146 cells in a dose-dependent manner. Moreover, we revealed that honokiol and magnolol could suppress signal transducer and activator of transcription (STAT)3 and protein kinase B (Akt) phosphorylation in IL-27-stimulated TR146 cells though STAT1 phosphorylation was not suppressed by honokiol and magnolol treatment. Furthermore, STAT3 and Akt inhibitors could suppress CXCR3 ligand production in TR146 cells. In summary, honokiol and magnolol could reduce CXCR3 ligand production in oral epithelial cell by inhibiting STAT3 and Akt activation.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10753-018-0854-z
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30039429; ● Search Scopus @ Elsevier (PMID): 30039429; ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-018-0854-z

(DOI: 10.1007/s10753-018-0854-z, PubMed: 30039429) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
Transforming growth factor-β1 increases C-C chemokine ligand 11 production in interleukin 4-stimulated human periodontal ligament cells.,
Cell Biology International, Vol.42, No.10, 1395-1400, 2018.

(要約): Transforming growth factor (TGF)-β1 is a multifunctional cytokine, which can control certain functions of various kinds of cells. However, it is unclear whether TGF-β1 affects T-cell migration in periodontal lesions. The aim of this study was to examine the effects of TGF-β1 on the production of C-C chemokine ligand (CCL)11, which is a T-helper 2-type chemokine, in human periodontal ligament cells (HPDLC). Interleukin (IL)-4 induced CCL11 production, but TGF-β1 did not, in HPDLC. However, TGF-β1 enhanced CCL11 production in IL-4-stimulated HPDLC. Western blot analysis showed that the signal transducer and activator of transcription 6 (STAT6) pathway was highly activated in HPDLC that had been stimulated with both IL-4 and TGF-β1. Mitogen-activated protein kinase activation did not differ between the HPDLC treated with a combination of IL-4 and TGF-β1 and those treated with IL-4 or TGF-β1 alone. Moreover, a STAT6 inhibitor significantly inhibited CCL11 production in HPDLC that had been stimulated with IL-4 and TGF-β1. The current study clearly demonstrated that TGF-β1 enhanced IL-4-induced CCL11 production in HPDLC. The STAT6 pathway is important for CCL11 production in IL-4- and TGF-β1-treated HPDLC.
(キーワード): Cells, Cultured / Chemokine CCL11 / Chemokines, CC / 細胞質分裂 (cytokinesis) / Humans / Interleukin-4 / Periodontal Ligament / リン酸化 (phosphorylation) / STAT6 Transcription Factor / シグナル伝達 (signal transduction) / Transforming Growth Factor beta1
(徳島大学機関リポジトリ): ● Metadata: 112813
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/cbin.11030
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 29993161; ● Search Scopus @ Elsevier (PMID): 29993161; ● Search Scopus @ Elsevier (DOI): 10.1002/cbin.11030

(徳島大学機関リポジトリ: 112813, DOI: 10.1002/cbin.11030, PubMed: 29993161) 細川義隆, 細川育子, 尾崎和美, 松尾敬志 :
テアフラビンが口腔上皮細胞のケモカイン産生に与える影響の解析,
日本歯科保存学雑誌, Vol.61, No.1, 10-16, 2018年.

(出版サイトへのリンク): ● Publication site (DOI): 10.11471/shikahozon.61.10
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390282680499546240; ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.61.10

(DOI: 10.11471/shikahozon.61.10, CiNii: 1390282680499546240) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
IL-27 Modulates Chemokine Production in TNF- -Stimulated Human Oral Epithelial Cells.,
Cellular Physiology and Biochemistry, Vol.43, No.3, 1198-1206, 2017.

(要約): IL-27 might control leukocyte migration in periodontal lesion by modulating chemokine production from epithelial cells.
(徳島大学機関リポジトリ): ● Metadata: 112954
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000481760
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28977795; ● Search Scopus @ Elsevier (PMID): 28977795; ● Search Scopus @ Elsevier (DOI): 10.1159/000481760

(徳島大学機関リポジトリ: 112954, DOI: 10.1159/000481760, PubMed: 28977795) Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo :
IL-29 Enhances CXCL10 Production in TNF--stimulated Human Oral Epithelial Cells.,
Immunological Investigations, Vol.46, No.6, 615-624, 2017.

(要約): Interleukin-29 (IL-29) is a cytokine belonging to the Type III interferon family. It was recently detected in the gingival crevicular fluid of periodontitis patients. However, the role of IL-29 in the pathogenesis of periodontal disease remains unknown. The aim of this study was to examine the effects of IL-29 on C-X-C motif chemokine ligand 10 (CXCL10) production in human oral epithelial cells. We measured CXCL10 production in TR146 cells, which is a human oral epithelial cell line, using an enzyme-linked immunosorbent assay. We used a Western blot analysis to detect IL-29 receptor expression and the phosphorylation levels of signal transduction molecules, including p38 mitogen-activated protein kinases (MAPK), signal transducer and activator of transcription 3 (STAT3), and nuclear factor (NF)- B p65, in the TR146 cells. The TR146 cells expressed the IL-29 receptor. IL-29 induced CXCL10 production in the TR146 cells. IL-29 significantly enhanced CXCL10 production in tumor necrosis factor (TNF)--stimulated TR146 cells. The p38 MAPK, STAT3, and NF-B pathways were found to be related to the IL-29-induced enhancement of CXCL10 production in TNF--stimulated TR146 cells. IL-29 promotes T helper 1-cell accumulation in periodontal lesions by inducing CXCL10 production in oral epithelial cells.
(徳島大学機関リポジトリ): ● Metadata: 112817
(出版サイトへのリンク): ● Publication site (DOI): 10.1080/08820139.2017.1336176
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 28753407; ● Search Scopus @ Elsevier (PMID): 28753407; ● Search Scopus @ Elsevier (DOI): 10.1080/08820139.2017.1336176

(徳島大学機関リポジトリ: 112817, DOI: 10.1080/08820139.2017.1336176, PubMed: 28753407) Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo :
Gomisin N Decreases Inflammatory Cytokine Production in Human Periodontal Ligament Cells.,
Inflammation, Vol.40, No.2, 360-365, 2017.

(要約): Gomisin N, which is a lignan isolated from Schisandra chinensis, has some pharmacological effects. However, the anti-inflammatory effects of gomisin N on periodontal disease are uncertain. The aim of this study was to examine the effect of gomisin N on inflammatory mediator production in tumor necrosis factor (TNF)--stimulated human periodontal ligament cells (HPDLC). Gomisin N inhibited interleukin (IL)-6, IL-8, CC chemokine ligand (CCL) 2, and CCL20 production in TNF--stimulated HPDLC in a dose-dependent manner. Moreover, we revealed that gomisin N could suppress extracellular signal-regulated kinase (ERK) and c-Jun N terminal kinase (JNK) phosphorylation in TNF--stimulated HPDLC though protein kinase B (Akt) phosphorylation was not suppressed by gomisin N treatment. In summary, gomisin N might exert anti-inflammatory effects by attenuating cytokine production in periodontal ligament cells via inhibiting the TNF--stimulated ERK and JNK pathways activation.
(キーワード): Anti-Inflammatory Agents / Cells, Cultured / Cyclooctanes / Cytokines / Dose-Response Relationship, Drug / Humans / Inflammation Mediators / Lignans / MAP Kinase Signaling System / Periodontal Ligament / Phosphorylation / Polycyclic Compounds / Tumor Necrosis Factor-alpha
(徳島大学機関リポジトリ): ● Metadata: 112816
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10753-016-0482-4
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27896541; ● Search Scopus @ Elsevier (PMID): 27896541; ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-016-0482-4

(徳島大学機関リポジトリ: 112816, DOI: 10.1007/s10753-016-0482-4, PubMed: 27896541) Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Yoshihiro Ohta, Kazumi Ozaki and Takashi Matsuo :
Alkannin inhibits CCL3 and CCL5 production in human periodontal ligament cells.,
Cell Biology International, Vol.40, No.12, 1380-1385, 2016.

(要約): Alkannin, which is found in Alkanna tinctoria, a member of the borage family, is used as a food coloring. Alkannin has recently been reported to have certain biological functions, such as anti-microbial and anti-oxidant effects. It is known that CC chemokine receptor (CCR) 5-positive leukocytes contribute to alveolar bone resorption in periodontal lesions. The aim of this study was to examine whether alkannin inhibits the production of CC chemokine ligand (CCL) 3 and CCL5, which are CCR5 ligands, in human periodontal ligament cells (HPDLC). Interleukin (IL)-1 induced CCL3 and CCL5 production in HPDLC. Alkannin inhibited IL-1-mediated CCL3 and CCL5 production in HPDLC in a dose-dependent manner. Moreover, we revealed that alkannin suppressed inhibitor of kappa B- degradation in IL-1-stimulated HPDLC. In addition, a nuclear factor (NF)-B inhibitor significantly inhibited CCL3 and CCL5 production in IL-1-stimulated HPDLC. These results demonstrate that alkannin inhibits CCR5 ligand production in IL-1-stimulated HPDLC by attenuating the NF-B signaling pathway.
(キーワード): Cells, Cultured / Chemokine CCL3 / Chemokine CCL5 / Humans / I-kappa B Proteins / Interleukin-1beta / Ligands / Naphthoquinones / Periodontal Ligament / リン酸化 (phosphorylation) / Proteolysis / Transcription Factor RelA
(徳島大学機関リポジトリ): ● Metadata: 112812
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/cbin.10692
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27743458; ● Search Scopus @ Elsevier (PMID): 27743458; ● Search Scopus @ Elsevier (DOI): 10.1002/cbin.10692

(徳島大学機関リポジトリ: 112812, DOI: 10.1002/cbin.10692, PubMed: 27743458) Ikuko Hosokawa, Yoshitaka Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo :
Melatonin Inhibits CXCL10 and MMP-1 Production in IL-1-Stimulated Human Periodontal Ligament Cells.,
Inflammation, Vol.39, No.4, 1520-1526, 2016.

(要約): Melatonin is a hormone that is mainly secreted by the pineal gland and exhibits a wide spectrum of activities, including antioxidant functions. Melatonin has been detected in gingival crevicular fluid. However, the role of melatonin in periodontal tissue is still uncertain. The aim of this study was to examine the effects of melatonin on inflammatory mediator expression in human periodontal ligament cells (HPDLC). Interleukin (IL)-1 induced CXC chemokine ligand (CXCL)10, matrix metalloproteinase (MMP)-1, and tissue inhibitors of metalloproteinase (TIMP)-1 production in HPDLC. Melatonin decreased CXCL10 and MMP-1 production and increased TIMP-1 production in IL-1-stimulated HPDLC. Western blot analysis showed that melatonin inhibited p38 mitogen-activated protein kinase (MAPK) and c-jun N-terminal kinase (JNK) phosphorylation, and IkB- degradation and phosphorylation in IL-1-stimulated HPDLC. These results suggest that melatonin might inhibit Th1 cell migration by reducing CXCL10 production. Moreover, melatonin might inhibit soft tissue destruction by decreasing MMP-1 production in periodontal lesions.
(徳島大学機関リポジトリ): ● Metadata: 112815
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10753-016-0386-3
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27271323; ● Search Scopus @ Elsevier (PMID): 27271323; ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-016-0386-3

(徳島大学機関リポジトリ: 112815, DOI: 10.1007/s10753-016-0386-3, PubMed: 27271323) Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
Shikonin Inhibits Inflammatory Cytokine Production in Human Periodontal Ligament Cells.,
Inflammation, Vol.39, No.3, 1124-1129, 2016.

(要約): Shikonin, which is derived from Lithospermum erythrorhizon, a herb used in traditional medicine, has long been considered to be a useful treatment for various diseases in traditional oriental medicine. Shikonin has recently been reported to have several pharmacological properties, e.g., it has anti-microbial, anti-tumor, and anti-inflammatory effects. The aim of this study was to examine whether shikonin is able to influence the production of interleukin (IL)-6, IL-8, and/or chemokine C-C motif ligand (CCL)20, which contribute to the pathogenesis of periodontal disease, in human periodontal ligament cells (HPDLC). The production levels of IL-6, IL-8, and CCL20 in HPDLC were determined using an ELISA. Western blot analysis was used to detect nuclear factor kappa B (NF-B) pathway activation in HPDLC. Shikonin prevented IL-1- or tumor necrosis factor (TNF)--mediated IL-6, IL-8, and CCL20 production in HPDLC. Moreover, we found that shikonin suppressed the phosphorylation and degradation of inhibitor of kappa B-alpha (IB-) in IL-1- or TNF--stimulated HPDLC. These findings suggest that shikonin could have direct beneficial effects against periodontal disease by reducing IL-6, IL-8, and CCL20 production in periodontal lesions.
(徳島大学機関リポジトリ): ● Metadata: 112814
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10753-016-0344-0
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27072015; ● Search Scopus @ Elsevier (PMID): 27072015; ● Search Scopus @ Elsevier (DOI): 10.1007/s10753-016-0344-0

(徳島大学機関リポジトリ: 112814, DOI: 10.1007/s10753-016-0344-0, PubMed: 27072015) Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo :
IL-4 Modulates CCL11 and CCL20 Productions from IL-1-Stimulated Human Periodontal Ligament Cells.,
Cellular Physiology and Biochemistry, Vol.38, No.1, 153-159, 2016.

(要約): These results mean that IL-4 enhanced Th2 cells migration in periodontal lesion to induce CCL11 production from HPDLCs. On the other hand, IL-4 inhibits Th17 cells accumulation in periodontally diseased tissues to inhibit CCL20 production. Therefore, IL-4 is positively related with the pathogenesis of periodontal disease to control chemokine productions in periodontal lesions.
(徳島大学機関リポジトリ): ● Metadata: 112953
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000438617
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26765337; ● Search Scopus @ Elsevier (PMID): 26765337; ● Search Scopus @ Elsevier (DOI): 10.1159/000438617

(徳島大学機関リポジトリ: 112953, DOI: 10.1159/000438617, PubMed: 26765337) Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo :
Calcitriol Suppressed Inflammatory Reactions in IL-1-Stimulated Human Periodontal Ligament Cells.,
Inflammation, Vol.38, No.6, 2252-2258, 2015.

(要約): Vitamin D has important roles on control of calcium and phosphate levels in the body. However, the role of vitamin D on the pathogenesis of periodontal disease is still uncertain. Therefore, we examined the effect of the hormonal form of vitamin D, calcitriol, on inflammatory responses of human periodontal ligament cells (HPDLC). We detected vitamin D receptor expression in non-stimulated HPDLC. Calcitriol inhibited interleukin (IL)-6, IL-8, CC chemokine ligand (CCL) 20, CXC chemokine ligand (CXCL) 10, and matrix metalloproteinase (MMP)-3 release from IL-1-stimulated HPDLC. Tissue inhibitor of metalloproteinase (TIMP)-1 production did not change by calcitriol. Moreover, we found c-jun N-terminal kinase (JNK) phosphorylation and IB- degradation in IL-1-stimulated HPDLC were inhibited by calcitriol, and JNK and nuclear factor (NF)-B inhibitors could decrease IL-6, IL-8, CCL20, CXCL10, and MMP-3 productions in IL-1-treated HPDLC. These findings suggest that vitamin D could modulate inflammatory response in periodontal tissues.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10753-015-0209-y
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 26156812; ● Summary page in Scopus @ Elsevier: 2-s2.0-84946497259

(DOI: 10.1007/s10753-015-0209-y, PubMed: 26156812, Elsevier: Scopus) Tadashi Nakanishi, Kayo Mukai, Yoshitaka Hosokawa, Daisuke Takegawa and Takashi Matsuo :
Catechins inhibit vascular endothelial growth factor production and cyclooxygenase-2 expression in human dental pulp cells,
International Endodontic Journal, Vol.48, No.3, 277-282, 2015.

(要約): To investigate the effect of catechins on vascular endothelial growth factor (VEGF) production and cyclooxygenase-2 (COX-2) expression in human dental pulp cells (HDPC) stimulated with bacteria-derived factors or pro-inflammatory cytokines. Morphologically fibroblastic cells established from explant cultures of healthy human dental pulp tissues were used as HDPC. HDPC pre-treated with catechins, epigallocatechin-3-gallate (EGCG) or epicatechin gallate (ECG), were exposed to lipopolysaccharide (LPS), peptidoglycan (PG), interlukin-1β (IL-1β) or tumour necrosis factor-α (TNF-α). VEGF production was examined by enzyme-linked immunosorbent assay, and COX-2 expression was assessed by immunoblot. EGCG and ECG significantly reduced LPS- or PG-mediated VEGF production in the HDPC in a dose-dependent manner. EGCG also prevented IL-1β-mediated VEGF production. Although TNF-α did not enhance VEGF production in the dental pulp cells, treatment of 20 μg mL(-1) of EGCG decreased the level of VEGF. In addition, the catechins attenuated COX-2 expression induced by LPS and IL-1β. The up-regulated VEGF and COX-2 expressions in the HDPC stimulated with these bacteria-derived factors or IL-1β were diminished by the treatment of EGCG and ECG. These findings suggest that the catechins may be beneficial as an anti-inflammatory tool of the treatment for pulpal inflammation.
(キーワード): catechin / cyclooxygenase-2 / dental pulp / vascular endothelial growth factor
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/iej.12312
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24847951; ● Search Scopus @ Elsevier (PMID): 24847951; ● Search Scopus @ Elsevier (DOI): 10.1111/iej.12312

(DOI: 10.1111/iej.12312, PubMed: 24847951) Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
Genipin inhibits MMP-1 and MMP-3 release from TNF--stimulated human periodontal ligament cells.,
Biochimie, Vol.107PB, 391-395, 2014.

(要約): Genipin, the aglycon of geniposide found in gardenia fruit has long been considered for treatment of inflammatory diseases in traditional oriental medicine. Genipin has recently been reported to have some pharmacological functions, such as antimicrobial, antitumor, and anti-inflammatory effects. The aim of this study was to examine whether genipin could modify matrix metalloproteinase (MMP)-1 and MMP-3, which are related to the destruction of periodontal tissues in periodontal lesion, expression in tumor necrosis factor (TNF)--stimulated human periodontal ligament cells (HPDLCs). Genipin prevented TNF--mediated MMP-1 and MMP-3 productions in HPDLCs. Moreover, genipin could suppress not only extracellular signal-regulated kinase (ERK) and Jun-N-terminal kinase (JNK) phosphorylations but also AMP-activated protein kinase (AMPK) phosphorylation in TNF--stimulated HPDLCs. Inhibitors of ERK and AMPK could inhibit both MMP-1 and MMP-3 productions. Moreover, we revealed the ERK inhibitor suppressed AMPK phosphorylation in TNF--stimulated HPDLCs. These data provide a new mechanism through which genipin could be used for the treatment of periodontal disease to prevent MMPs expression in periodontal lesion.
(徳島大学機関リポジトリ): ● Metadata: 110103
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.biochi.2014.10.008
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25457105; ● Summary page in Scopus @ Elsevier: 2-s2.0-84915753375

(徳島大学機関リポジトリ: 110103, DOI: 10.1016/j.biochi.2014.10.008, PubMed: 25457105, Elsevier: Scopus) Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo :
IL-22 Enhances CCL20 Production in IL-1-Stimulated Human Gingival Fibroblasts.,
Inflammation, Vol.37, No.6, 2062-2066, 2014.

(要約): CC chemokine ligand 20 (CCL20) is involved in the recruitment of Th17 cells and thus in the exacerbation of periodontal disease, but the effect of simultaneous interleukin (IL)-22 and IL-1 stimulation on CCL20 production in human gingival fibroblasts (HGFs) is uncertain. In this study, we investigated the mechanisms of IL-1- and/or IL-22-induced CCL20 production in HGFs. A single stimulation of IL-22 could not induce CCL20 production. On the other hand, IL-22 could increase CCL20 production from IL-1-stimulated HGFs in a dose-dependent manner. C-Jun N terminal kinase (JNK) and inhibitor of nuclear factor B (IB)- phosphorylation were increased in IL-1- and IL-22-stimulated HGFs. An inhibitor of nuclear factor (NF)-B decreased IL-1- and IL-22-induced CCL20 production, though an inhibitor of JNK did not modulate CCL20 production. These data suggest that IL-1 in cooperation with IL-22 could increase Th17 cell accumulation in periodontally diseased tissues to enhance CCL20 production in HGFs.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10753-014-9939-5
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24902798; ● Summary page in Scopus @ Elsevier: 2-s2.0-84937557635

(DOI: 10.1007/s10753-014-9939-5, PubMed: 24902798, Elsevier: Scopus) Yoshitaka Hosokawa, Satoru Shindo, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
IL-6 trans-signaling enhances CCL20 production from IL-1-stimulated human periodontal ligament cells.,
Inflammation, Vol.37, No.2, 381-386, 2014.

(要約): CC chemokine ligand 20 (CCL20) plays a central role in the recruitment of CCR6-expressing cells, including Th17 cells which are related to bone resorption in periodontal lesions and thus in the development of periodontal disease. IL-6 is an important cytokine that is associated with the pathogenesis of periodontitis. However, the effect of IL-6 on CCL20 production is uncertain. The aim of this study was to examine whether IL-6 could modify CCL20 expression in human periodontal ligament cells (HPDLCs). HPDLCs expressed gp130 but did not express IL-6R on the surface of HPDLCs. So, IL-6 trans-signaling is important to recognize IL-6 by HPDLCs. IL-6/sIL-6R stimulation enhanced CCL20 production in IL-1-stimulated HPDLCs. IL-6 produced from IL-1-stimulated HPDLCs with sIL-6R could increase CCL20 production in HPDLCs with sIL-6R. Signal transducer and activator of transcription (STAT)3 activation was related to CCL20 production in IL-1 and IL-6/sIL-6R-stimulated HPDLCs. Our data suggests that HPDLCs, in response to IL-6, sIL-6R, and IL-1, may shift chemokine production to that favoring CCR6-expressing cells recruitment in periodontal lesions.
(出版サイトへのリンク): ● Publication site (DOI): 10.1007/s10753-013-9750-8
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24081898; ● Summary page in Scopus @ Elsevier: 2-s2.0-84896326562

(DOI: 10.1007/s10753-013-9750-8, PubMed: 24081898, Elsevier: Scopus) Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
Genipin inhibits IL-1-induced CCL20 and IL-6 production from human periodontal ligament cells.,
Cellular Physiology and Biochemistry, Vol.33, No.2, 357-364, 2014.

(要約): These data provide a novel mechanism through which genipin could be used to provide direct benefits in periodontal disease to inhibit IL-6 and CCL20 productions in periodontal lesions.
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000356675
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24557363; ● Summary page in Scopus @ Elsevier: 2-s2.0-84895641086

(DOI: 10.1159/000356675, PubMed: 24557363, Elsevier: Scopus) Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo :
(-)-Epigallocatechin-3-Gallate Inhibits CC Chemokine Ligand 11 Production in Human Gingival Fibroblasts.,
Cellular Physiology and Biochemistry, Vol.31, No.6, 960-967, 2013.

(要約): Background: CC chemokine ligand 11 (CCL11) is related to Th2 cells migration via CC chemokine receptor 3 (CCR3). Th2 cells are involved in the etiology of periodontal disease. However, how the infiltration of Th2 cells is controlled in periodontally diseased tissues is unknown. (-)-Epigallocatechin gallate (EGCG), the major catechin in green tea, has multiple beneficial effects, but the effects of EGCG on CCL11 production are uncertain. In this study, we investigated whether cytokines could induce CCL11 production in human gingival fibroblasts (HGFs). Moreover, we examined the effects of EGCG on CCL11 production in HGFs. Methods and Results: ELISA analysis disclosed that interleukin (IL)-4 synergistically enhanced CCL11 production in IL-1 or tumor necrosis factor (TNF)--stimulated HGFs. EGCG prevented IL-1/ IL-4 or TNF-/IL-4-mediated CCL11 production in a concentration dependent manner. CCL11 production in HGFs was positively regulated by p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), and c-Jun N terminal kinase (JNK). Western blot analysis revealed that EGCG treatment prevented IL-1/IL-4 or TNF-/IL-4-induced ERK and JNK activation in HGFs. Conclusions: These data provide that CCL11 production in HGFs could be associated with Th2 cells infiltration in periodontal lesions. Moreover, EGCG is useful for periodontitis treatment to inhibit CCL11 production.
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000350114
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23839108; ● Search Scopus @ Elsevier (PMID): 23839108; ● Search Scopus @ Elsevier (DOI): 10.1159/000350114

(DOI: 10.1159/000350114, PubMed: 23839108) Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo :
TLR3 agonist enhances CC chemokine ligand 20 production in IL-1-stimulated human gingival fibroblasts.,
Cellular Immunology, Vol.283, No.1-2, 8-11, 2013.

(要約): Viruses are related to the etiology of periodontitis. However, the role of viruses on Th17 cells infiltration in periodontitis lesions is unknown. Therefore, we examined the effects of TLR3 ligand on CCL20, which is related to Th17 cells migration, production in human gingival fibroblasts (HGFs). Polyinosinic-polycytidylic acid (Poly I:C), which is a TLR3 agonist, stimulation could moderately induce CCL20 production in HGFs. Poly I:C synergistically enhanced CCL20 expression from IL-1-stimulated HGFs. Inhibitors of p38 MAPK, extracellular signal-regulated kinase (ERK), c-Jun N terminal kinase (JNK), and NF-B significantly inhibited CCL20 production in Poly I:C/IL-1-stimulated HGFs. Western blot analysis disclosed phosphorylation of p38 MAPK, JNK, and IB- were enhanced in Poly I:C/IL-1-treated HGFs. These data suggested that virus infection is related to Th17 cells migration in periodontitis lesion to induce CCL20 production in HGFs via TLR3. Therefore, our results indicated that virus might be important pathogen in periodontal disease.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.cellimm.2013.05.005
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23850670; ● Search Scopus @ Elsevier (PMID): 23850670; ● Search Scopus @ Elsevier (DOI): 10.1016/j.cellimm.2013.05.005

(DOI: 10.1016/j.cellimm.2013.05.005, PubMed: 23850670) Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Tumor necrosis factor-like weak inducer of apoptosis increases CC chemokine ligand 20 production in interleukin 1-stimulated human gingival fibroblasts.,
Human Immunology, Vol.73, No.5, 470-473, 2012.

(要約): CC chemokine ligand 20 (CCL20) is related to T-helper (Th)-17 cell migration, and Th17 cells play important roles in exacerbation in periodontal disease. However, the effect of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) on CCL20 production is unknown. In this study, we examined the mechanisms of TWEAK in combination with interleukin (IL)-1-induced CCL20 production in human gingival fibroblasts (HGFs). TWEAK alone did not induce CCL20 production in HGFs. However, TWEAK enhanced CCL20 expression from IL-1-stimulated HGFs in a dose-dependent manner. Inhibitors of p38 mitogen-activated protein kinase, extracellular signal-regulated kinase (ERK), protein kinase B (Akt), and nuclear factor B (NF-B) significantly inhibited CCL20 production in TWEAK and IL-1-stimulated HGFs. Western blot analysis revealed that phosphorylations of ERK, Akt, and inhibitor of NF-B were enhanced in TWEAK and IL-1-treated HGFs. These data suggest that TWEAK is positively related to Th17 cell migration in periodontally diseased tissues to enhance CCL20 production in IL-1-stimulated HGFs.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.humimm.2012.02.021
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22425737; ● Search Scopus @ Elsevier (PMID): 22425737; ● Search Scopus @ Elsevier (DOI): 10.1016/j.humimm.2012.02.021

(DOI: 10.1016/j.humimm.2012.02.021, PubMed: 22425737) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Interleukin (IL)-17A synergistically enhances CC chemokine ligand 20 production in IL-1-stimulated human gingival fibroblasts.,
Human Immunology, Vol.73, No.1, 26-30, 2012.

(要約): CC chemokine ligand 20 (CCL20) plays a pivotal role in the recruitment of T-helper (Th)-17 cells and thus in the development of periodontal disease, but the effect of simultaneous interleukin (IL)-17A and IL-1 stimulation on CCL20 production in human gingival fibroblasts (HGFs) are not known. In this study, we investigated the mechanisms of IL-1- and IL-17A-induced CCL20 production in HGFs. IL-17A synergistically enhanced CCL20 production from IL-1-stimulated HGFs in a concentration-dependent manner. Extracellular signal-regulated kinase (ERK) and inhibitor of nuclear factor (NF)-B- phosphorylation were increased in IL-1- and IL-17A-stimulated HGFs. Inhibitors of or ERK and NF-B decreased IL-1- and IL-17A-induced CCL20 production. IL-1 stimulation elevated IL-17 receptor C expression on HGFs. These data suggest that IL-1 is actively related to Th17 cell migration into peripheral tissues to induce production of the Th17 chemokine, CCL20. Therefore, IL-1 might be a therapeutic target for Th17-related diseases, such as periodontal disease and arthritis.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.humimm.2011.10.004
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22019504; ● Search Scopus @ Elsevier (PMID): 22019504; ● Search Scopus @ Elsevier (DOI): 10.1016/j.humimm.2011.10.004

(DOI: 10.1016/j.humimm.2011.10.004, PubMed: 22019504) Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo :
Black tea polyphenol inhibits CXCL10 production in oncostatin M-stimulated human gingival fibroblasts.,
International Immunopharmacology, Vol.11, No.6, 670-674, 2011.

(要約): CXC chemokine ligand 10 (CXCL10) plays an important role in the infiltration of Th1 cells and thus in the exacerbation of periodontal disease. Theaflavin-3,3'-digallate (TFDG), polyphenol in black tea, has some beneficial effects but the effect of TFDG on CXCL10 production from human gingival fibroblasts (HGFs) is uncertain. In this study, we investigated the mechanisms by which TFDG may inhibit oncostatin M (OSM)-induced CXCL10 production in human gingival fibroblasts. TFDG prevented OSM-mediated CXCL10 production by HGFs in a dose dependent manner. TFDG significantly inhibited OSM-induced phosphorylation of c-Jun N terminal kinase (JNK), protein kinase B (Akt) (Ser473) that are related to CXCL10 production from OSM-stimulated HGFs. In addition, TFDG suppressed OSM receptor (OSMR) β expression on HGFs. These data provide a novel mechanism where the black tea flavonoid, theaflavin, could provide direct benefits in periodontal disease.
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.intimp.2011.01.009
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21255696; ● Search Scopus @ Elsevier (PMID): 21255696; ● Search Scopus @ Elsevier (DOI): 10.1016/j.intimp.2011.01.009

(DOI: 10.1016/j.intimp.2011.01.009, PubMed: 21255696) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Oncostatin M synergistically induces CXCL10 and ICAM-1 expression in IL-1beta-stimulated-human gingival fibroblasts.,
Journal of Cellular Biochemistry, Vol.111, No.1, 40-48, 2010.

(要約): Periodontitis is a chronic bacterial infection of tooth-supporting structures. T-helper type 1 (Th1) cells are related to the exacerbation of periodontal disease. Human gingival fibroblasts (HGFs), the major cell type in periodontal connective tissues, are involved in immunological response in periodontal tissues. However, it is uncertain whether HGFs are related to Th1 response. Chemokine (C-X-C motif) ligand 10 (CXCL10) is a cytokine, that is related to Th1 cells migration. Intercellular adhesion molecule (ICAM)-1 is involved in Th1 cells retention and activation in inflamed tissue. The aim of this study is to examine the effect of oncostatin M (OSM) on CXCL10 and ICAM-1 expression in HGFs. OSM stimulation induced CXCL10 and ICAM-1 expression in HGFs. Moreover, the synergistic effects of CXCL10 release and ICAM-1 expression in HGFs were observed with combined stimulation of interleukin (IL)-1beta and OSM. OSM increased type 1 IL-1 receptor (IL-1R1) expression, and IL-1beta enhanced OSMRbeta expression on HGFs. IL-1beta + OSM stimulation enhanced the phosphorylation of inhibitor of nuclear factor kappaB (IkappaB)-alpha, signal transducer and activator of transcription (STAT)3, c-Jun N terminal kinase (JNK), and protein kinase B (Akt) compared to OSM or IL-1beta stimulation. CXCL10 production from OSM + IL-1beta stimulated HGFs was suppressed by nuclear factor (NF)-kappaB, STAT3, JNK, and phosphoinositide-3-kinase (PI3K) inhibitors. On the other hand, only NF-kappaB and STAT3 inhibitors suppressed ICAM-1 expression enhanced by OSM + IL-1beta treatment. These effects of OSM and IL-1beta may promote Th1 cells infiltration and retention in periodontally diseased tissues and be related to exacerbation of periodontal disease. J. Cell. Biochem. 111: 40-48, 2010. (c) 2010 Wiley-Liss, Inc.
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/jcb.22648
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20680966; ● Search Scopus @ Elsevier (PMID): 20680966; ● Search Scopus @ Elsevier (DOI): 10.1002/jcb.22648

(DOI: 10.1002/jcb.22648, PubMed: 20680966) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo :
Tea polyphenols inhibit IL-6 production in tumor necrosis factor superfamily 14-stimulated human gingival fibroblasts.,
Molecular Nutrition & Food Research, Vol.54 Suppl 2, S151-8, 2010.

(要約): IL-6 is well recognized to be a potent bone resorptive agent and thus in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins in green tea, and theaflavin-3,3'-digallate (TFDG), polyphenol in black tea, have multiple beneficial effects, but the effects of catechins and theaflavins on IL-6 production in human gingival fibroblasts (HGFs) are not known. In this study, we investigated the mechanisms by which EGCG, ECG, and TFDG inhibit tumor necrosis factor superfamily 14 (TNFSF14)-induced IL-6 production in HGFs. We detected TNFSF14 mRNA expression in human diseased periodontal tissues. TNFSF14 increased IL-6 production in HGFs in a concentration-dependent manner. EGCG, ECG, and TFDG prevented TNFSF14-mediated IL-6 production in HGFs. EGCG, ECG, and TFDG prevented TNFSF14-induced extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nuclear factor-kappaB activation in HGFs. Inhibitors of ERK, JNK, and nuclear factor-kappaB decreased TNFSF14-induced IL-6 production. In addition, EGCG, ECG, and TFDG attenuated TNFSF14 receptor expression on HGFs. These data provide a novel mechanism through which the green tea and black tea polyphenols could be used to provide direct benefits in periodontal disease.
(出版サイトへのリンク): ● Publication site (DOI): 10.1002/mnfr.200900549
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20461739; ● Search Scopus @ Elsevier (PMID): 20461739; ● Search Scopus @ Elsevier (DOI): 10.1002/mnfr.200900549

(DOI: 10.1002/mnfr.200900549, PubMed: 20461739) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo :
Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts,
The Journal of Nutritional Biochemistry, Vol.21, No.7, 659-664, 2010.

(要約): CXC chemokine ligand 10 (CXCL10) plays a pivotal role in the recruitment of Th1 cells and, thus, in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins derived from green tea, have multiple beneficial effects, but the effects of catechins on CXCL10 production from human gingival fibroblasts (HGFs) is not known. In this study, we investigated the mechanisms by which EGCG and ECG inhibit oncostatin M (OSM)-induced CXCL10 production in HGFs. HGFs constitutively expressed glycoprotein 130 and OSM receptor beta (OSMR beta), which are OSM receptors. OSM increased CXCL10 production in a concentration-dependent manner. EGCG and ECG prevented OSM-mediated CXCL10 production by HGFs. Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription (STAT)3 decreased OSM-induced CXCL10 production. EGCG significantly prevented OSM-induced phosphorylation of JNK, Akt (Ser473) and STAT3 (Tyr705 and Ser727). ECG prevented phosphorylation of JNK and Akt (Ser473). In addition, EGCG and ECG attenuated OSMR beta expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids, catechins, can provide direct benefits in periodontal disease.
(キーワード): Anti-Inflammatory Agents, Non-Steroidal / Antioxidants / Catechin / Cells, Cultured / Chemokine CXCL10 / Cytokine Receptor gp130 / Enzyme Inhibitors / Fibroblasts / Gene Expression Regulation / Gingiva / Humans / Oncostatin M / Oncostatin M Receptor beta Subunit / Osmolar Concentration / Periodontal Diseases / Phosphorylation / Signal Transduction
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.jnutbio.2009.04.005
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19616927; ● Search Scopus @ Elsevier (PMID): 19616927; ● Search Scopus @ Elsevier (DOI): 10.1016/j.jnutbio.2009.04.005

(DOI: 10.1016/j.jnutbio.2009.04.005, PubMed: 19616927) Tadashi Nakanishi, Kayo Mukai, Hiromichi Yumoto, Kouji Hirao, Yoshitaka Hosokawa and Takashi Matsuo :
Anti-inflammatory effect of catechin on cultured dental pulp cells affected by bacteria-derived factors,
European Journal of Oral Sciences, Vol.118, No.2, 145-150, 2010.

(要約): Catechins (bioactive polyphenols in green tea) are known to exhibit potent anti-inflammatory properties. However, the anti-inflammatory effects of catechins on inflamed dental pulp tissue are not known. In this study, we investigated the effect of epigallocatechin-3-gallate (EGCG) and epicatechin gallate (ECG), the major components of green tea catechins, on the expression of pro-inflammatory cytokines and adhesion molecules in human dental pulp cells stimulated with bacteria-derived factors such as lipopolysaccharide (LPS) and peptidoglycan (PG). The expression of interleukin (IL)-6 and of IL-8 was examined using the reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assays. The expression of intercellular adhesion molecule-1 (ICAM-1) and of vascular cell adhesion molecule-1 (VCAM-1) on dental pulp cells was analyzed using flow cytometry. The presence of EGCG and ECG significantly reduced, in a concentration-dependent manner, the expression of IL-6 and IL-8 in dental pulp cells exposed to LPS or PG. Increased expression of ICAM-1 and VCAM-1 on the dental pulp cells in response to bacterial components was also decreased by treatment with EGCG and ECG. These findings suggest that green tea catechins may prevent the exacerbation of pulpitis.
(キーワード): Anti-Inflammatory Agents / Antioxidants / Catechin / Cells, Cultured / Dental Pulp / Escherichia coli / Flow Cytometry / Humans / Intercellular Adhesion Molecule-1 / Interleukin-6 / Interleukin-8 / Lipopolysaccharides / Peptidoglycan / Reverse Transcriptase Polymerase Chain Reaction / Staphylococcus aureus / Time Factors / Vascular Cell Adhesion Molecule-1
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1600-0722.2010.00714.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20487003; ● Search Scopus @ Elsevier (PMID): 20487003; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0722.2010.00714.x

(DOI: 10.1111/j.1600-0722.2010.00714.x, PubMed: 20487003) Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hiromichi Yumoto, Hideaki Nakae and Takashi Matsuo :
Proinflammatroy effects of muramyldipeptide on human gingival fibroblasts,
Journal of Periodontal Research, Vol.45, No.2, 193-199, 2010.

(要約): Because human gingival fibroblasts (HGFs) are the predominant cells in periodontal tissues, we hypothesized that HGFs are contributed to receptors for components of bacteria. In this study, we focused on expression and function of nucleotide binding oligomerization domain 2 (NOD2) in HGFs, which is a mammalian cytosolic pathogen recognition molecule. Expression of NOD2 in HGFs was examined by reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry. Production of interleukin (IL)-6, IL-8, cc chemokine ligand2, cxc chemokine ligand10 (CXCL10) and CXCL11 from HGFs was examined by enzyme-linked immunosorbent assay (ELISA). We used RT-PCR and immunohistochemistry to detect the NOD2 expression in human gingival tissues. We found clear NOD2 expression in HGFs. Upon stimulation with NOD2 agonist, muramyldipeptide (MDP), production of proinflammatory cytokines was enhanced. Moreover, MDP-induced production of proinflammatory cytokines was inhibited in a different manner by mitogen-activated protein kinase inhibitors and phosphatidylinositol 3-kinase inhibitor. Furthermore, MDP enhanced CXCL10 and CXCL11 productions by tumor necrosis factor-alpha (TNF-alpha)- or interferon-gamma (IFN-gamma)-stimulated HGFs, although MDP alone did not induce these chemokines. TNF-alpha and IFN-gamma increased NOD2 expression in HGFs. In addition, we detected NOD2 expression in mononuclear cells and HGFs in periodontally diseased tissues. These findings indicate that MDP which induces production of cytokines and chemokines from HGFs is related to the pathogenesis of periodontal disease.
(キーワード): Acetylmuramyl-Alanyl-Isoglutamine / Adult / Anthracenes / Calcium-Calmodulin-Dependent Protein Kinases / Cells, Cultured / Chemokine CCL2 / Chemokine CXCL10 / Chemokine CXCL11 / Chromones / Chronic Periodontitis / Enzyme Inhibitors / Female / Fibroblasts / Flavonoids / Gingiva / Humans / Imidazoles / Inflammation Mediators / Interferon-gamma / Interleukin-6 / Interleukin-8 / JNK Mitogen-Activated Protein Kinases / Male / Middle Aged / Morpholines / Nod2 Signaling Adaptor Protein / Periodontal Attachment Loss / Periodontal Pocket / Phosphatidylinositol 3-Kinases / Pyridines / Tumor Necrosis Factor-alpha
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1600-0765.2009.01217.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20470259; ● Search Scopus @ Elsevier (PMID): 20470259; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2009.01217.x

(DOI: 10.1111/j.1600-0765.2009.01217.x, PubMed: 20470259) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
TNFSF14 coordinately enhances CXCL10 and CXCL11 production from IFN-gamma-stimulated human gingival fibroblasts,
Molecular Immunology, Vol.47, No.4, 666-670, 2010.

(要約): TNFSF14 is involved in the pathogenesis of some inflammatory diseases such as arthritis. CXCL10 and CXCL11 recruit Th1 cells, and the productions of these chemokines are related to the exacerbation of some inflammatory diseases including arthritis and periodontal disease. We examined in vitro effects of TNFSF14 on IFN-gamma-induced CXCL10 and CXCL11 production in human gingival fibroblasts (HGFs). HGFs constitutively expressed TNFSF14 receptors, LTbetaR and HVEM. TNFSF14 enhanced IFN-gamma-induced secretion of CXCL10 and CXCL11 from HGFs. IFN-gamma treatment increased HVEM expression on HGFs. TNFSF14 in combination with IFN-gamma resulted in increased activation of p38 MAPK, ERK and IkappaB-alpha compared with TNFSF14 or IFN-gamma alone. Moreover, inhibitors of p38 MAPK, ERK and NF-kappaB abolished the CXCL10 and CXCL11 productions from TNFSF14 with IFN-gamma-stimulated HGFs. These effects of TNFSF14 may promote the infiltration of Th1 cells into lesions with inflammatory diseases. TNFSF14 might act as a proinflammatory cytokine in some inflammatory diseases thus is a candidate therapeutic target.
(キーワード): Chemokine CXCL10 / Chemokine CXCL11 / Extracellular Signal-Regulated MAP Kinases / Fibroblasts / Gingiva / Humans / I-kappa B Proteins / Interferon-gamma / Lymphotoxin beta Receptor / MAP Kinase Kinase Kinases / Phosphorylation / Protein Kinase Inhibitors / Proto-Oncogene Proteins / RNA, Messenger / Receptors, Tumor Necrosis Factor, Member 14 / Signal Transduction / Tumor Necrosis Factor Ligand Superfamily Member 14 / Up-Regulation
(出版サイトへのリンク): ● Publication site (DOI): 10.1016/j.molimm.2009.10.018
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19939453; ● Search Scopus @ Elsevier (PMID): 19939453; ● Search Scopus @ Elsevier (DOI): 10.1016/j.molimm.2009.10.018

(DOI: 10.1016/j.molimm.2009.10.018, PubMed: 19939453) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo :
Catechins Inhibit CCL20 Production in IL-17A-stimulated Human Gingival Fibroblasts,
Cellular Physiology and Biochemistry, Vol.24, No.5-6, 391-396, 2009.

(要約): CC chemokine ligand 20 (CCL20) plays a pivotal role in the recruitment of Th17 cells and thus in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins in green tea, have multiple beneficial effects, but the effects of catechins on CCL20 production in human gingival fibroblasts (HGFs) are not known. In this study, we investigated the mechanisms by which EGCG and ECG inhibit interleukin (IL)-17A-induced CCL20 production in human gingival fibroblasts. IL-17A increased CCL20 production in HGFs in a concentration-dependent manner. EGCG and ECG prevented IL-17A-mediated CCL20 production in HGFs. Inhibitors of p38 mitogen-activated protein kinase (MAPK) or extracellular signal-regulated kinase (ERK) decreased IL-17A-induced CCL20 production. EGCG and ECG prevented IL-17A-induced phosphorylation of p38 MAPK and ERK in HGFs. In addition, EGCG and ECG attenuated IL-17 receptor expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids catechins could be used to provide direct benefits in periodontal disease.
(キーワード): Antioxidants / Catechin / Cells, Cultured / Chemokine CCL20 / Extracellular Signal-Regulated MAP Kinases / Fibroblasts / Gingiva / Humans / Interleukin-17 / Phosphorylation / p38 Mitogen-Activated Protein Kinases
(出版サイトへのリンク): ● Publication site (DOI): 10.1159/000257431
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19910679; ● Search Scopus @ Elsevier (PMID): 19910679; ● Search Scopus @ Elsevier (DOI): 10.1159/000257431

(DOI: 10.1159/000257431, PubMed: 19910679) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Human gingival fibroblasts express functional chemokine receptor CXCR6.,
Clinical and Experimental Immunology, Vol.156, No.3, 413-418, 2009.

(要約): We have reported that CXCL16, a recently discovered transmembrane chemokine, is expressed in human gingival fibroblasts (HGF). However, it is not known whether HGF express CXCR6, the receptor for CXCL16, or CXCL16 affects HGF biology. We have shown that HGF expressed CXCR6 by reverse transcription-polymerase chain reaction and flow cytometric analysis. Moreover, we elucidated that tumour necrosis factor (TNF)-alpha and cytosine-guanine dinucleotide (CpG) DNA (Toll-like receptor-9 ligand) treatment enhanced CXCR6 expression by HGF. Interleukin (IL)-4, IL-13 and CpG DNA up-regulated CXCR6 expression by TNF-alpha-stimulated HGF. On the other hand, IL-1beta and interferon-gamma inhibited CXCR6 expression on TNF-alpha-treated HGF. CXCL16 treatment induced HGF proliferation and phosphorylation of extracellular regulated kinase (ERK) and protein kinase B (AKT) in HGF. In conclusion, HGF expressed CXCR6 functionally, because CXCL16 induced HGF proliferation and ERK and AKT phosphorylation in HGF. These results indicate that CXCL16 may play an important role in the pathogenesis and remodelling in periodontally diseased tissues.
(キーワード): Cell Proliferation / Cells, Cultured / Chemokines, CXC / CpG Islands / Cytokines / Extracellular Signal-Regulated MAP Kinases / Fibroblasts / Gingiva / Humans / Ligands / Proto-Oncogene Proteins c-akt / Receptors, Chemokine / Receptors, Scavenger / Receptors, Virus / Reverse Transcriptase Polymerase Chain Reaction / Toll-Like Receptors
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2249.2009.03915.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19438592; ● Search Scopus @ Elsevier (PMID): 19438592; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2009.03915.x

(DOI: 10.1111/j.1365-2249.2009.03915.x, PubMed: 19438592) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Cytokines differentially regulate CXCL10 production by interferon-gamma-stimulated or tumor necrosis factor-alpha-stimulated human gingival fibroblasts.,
Journal of Periodontal Research, Vol.44, No.2, 225-231, 2009.

(要約): CXC chemokine 10 (CXCL10) activates CXC chemokine receptor 3 (CXCR3) and attracts activated T-helper 1 cells. In this study we examined the effects of cytokines on CXCL10 production by human gingival fibroblasts. Human gingival fibroblasts were exposed to pro-inflammatory cytokines (interleukin-1beta, tumor necrosis factor-alpha), a T-helper 1 cytokine (interferon-gamma), T-helper 2 cytokines (interleukin-4, interleukin-13), T-helper 17 cytokines (interleukin-17A, interleukin-22) and regulatory T-cell cytokines (interleukin-10, transforming growth factor-beta1) for 24 h. CXCL10 production by human gingival fibroblasts was examined by enzyme-linked immunosorbent assay. Human gingival fibroblasts produced CXCL10 protein upon stimulation with interleukin-1beta, tumor necrosis factor-alpha and interferon-gamma. Treatment of human gingival fibroblasts with interferon-gamma in combination with tumor necrosis factor-alpha or interleukin-1beta resulted in a synergistic production of CXCL10. However, interleukin-4 and interleukin-13 inhibited CXCL10 production by interferon-gamma-stimulated or tumor necrosis factor-alpha-stimulated-human gingival fibroblasts. On the other hand, interleukin-17A and interleukin-22 enhanced CXCL10 production by human gingival fibroblasts treated with interferon-gamma and inhibited CXCL10 production by tumor necrosis factor-alpha-stimulated human gingival fibroblasts. Furthermore, the anti-inflammatory cytokine, interleukin-10, inhibited CXCL10 production by both interferon-gamma- and tumor necrosis factor-alpha-stimulated human gingival fibroblasts, but transforming growth factor-beta1 enhanced interferon-gamma-mediated CXCL10 production by human gingival fibroblasts. These results mean that the balance of cytokines in periodontally diseased tissue may be essential for the control of CXCL10 production by human gingival fibroblasts, and the production of CXCL10 might be important for the regulation of T-helper 1 cell infiltration in periodontally diseased tissue.
(キーワード): Adult / Cells, Cultured / Chemokine CXCL10 / Cytokines / Female / Fibroblasts / Gingiva / Humans / Inflammation Mediators / Interferon-gamma / Interleukins / Periodontitis / Th1 Cells / Transforming Growth Factor beta1 / Tumor Necrosis Factor-alpha
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1600-0765.2008.01124.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18973545; ● Search Scopus @ Elsevier (PMID): 18973545; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2008.01124.x

(DOI: 10.1111/j.1600-0765.2008.01124.x, PubMed: 18973545) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
CC Chemokine ligand 17 in periodontal diseases: expression in diseased tissues and production by human gingival fibroblasts,
Journal of Periodontal Research, Vol.43, No.4, 471-477, 2008.

(要約): It has been reported that T helper 2 (Th2) cells are related to exacerbation of periodontal disease. However, it is uncertain how the migration of Th2 cells is controlled. In this study, we examined the expression of CC chemokine ligand 17 (CCL17), which is a Th2 chemokine, in periodontal tissues. Moreover, we investigated the effects of cytokines and toll-like receptor (TLR) ligands on the production of CCL17 by human gingival fibroblasts (HGFs). We used immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) to detect CCL17 in periodontal tissues. HGFs were exposed to cytokines and TLR ligands. Expression of CCL17 was examined by RT-PCR and enzyme-linked immunosorbent assay. We used signal transduction inhibitors in some experiments. Both CCL17 and its receptor, CC chemokine receptor 4 (CCR4), were expressed in diseased periodontal tissues. A combination of tumour necrosis factor alpha (TNF-alpha) and interleukin (IL)-4/IL-13 increased CCL17 expression. Moreover, treatment of HGFs with a low dose of interferon-gamma (IFN-gamma) in combination with TNF-alpha and IL-4 or IL-13 had synergistic effects on the production of CCL17, whereas a high dose of IFN-gamma inhibited CCL17 production. Furthermore, Escherichia coli (E. coli) lipopolysaccharide (TLR4 ligand) and Pam3CSK4 (TLR2 ligand) inhibited CCL17 production by TNF-alpha + IL-4-stimulated HGFs, while CpG DNA (TLR9 ligand) enhanced TNF-alpha + IL-4 induced-CCL17 production by HGFs. Furthermore, a c-Jun NH2 terminal kinase (JNK) inhibitor, a phosphatidylinositol-3-kinase (PI3K) inhibitor and a nuclear factor kappa B (NF-kappa B) inhibitor inhibited CCL17 production by HGFs. These results suggest that the CCL17 produced by HGFs may be involved in the migration of Th2 cells into inflamed tissues, and provide evidence that CCL17 production is controlled by cytokines and TLR ligands in periodontal disease.
(キーワード): Chemokine CCL17 / Cytokines / Escherichia coli / Fibroblasts / Gingiva / Humans / Interferon-gamma / Interleukin-13 / Interleukin-4 / JNK Mitogen-Activated Protein Kinases / Ligands / Lipopeptides / Lipopolysaccharides / NF-kappa B / Peptides / Periodontal Diseases / Phosphatidylinositol 3-Kinases / Receptors, CCR4 / Reverse Transcriptase Polymerase Chain Reaction / Th2 Cells / Toll-Like Receptor 2 / Toll-Like Receptor 4 / Toll-Like Receptor 9 / Toll-Like Receptors / Tumor Necrosis Factor-alpha
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1600-0765.2007.01080.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18557811; ● Search Scopus @ Elsevier (PMID): 18557811; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0765.2007.01080.x

(DOI: 10.1111/j.1600-0765.2007.01080.x, PubMed: 18557811) Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Adrenomedullin suppresses tumour necrosis factor alpha-induced CXC chemokine ligand 10 production by human gingival fibroblasts.,
Clinical and Experimental Immunology, Vol.152, No.3, 568-575, 2008.

(要約): Periodontal disease is an inflammatory disorder characterized by the involvement of chemokines that are important for the recruitment of leucocytes. Several cytokines, including tumour necrosis factor alpha (TNF-alpha), are involved in regulating levels of chemokines in periodontal disease. CXC chemokine ligand 10 (CXCL10) is a chemokine related to the migration of T helper 1 cells. In this study, we examined CXCL10 expression in human gingival fibroblasts (HGFs). Moreover, we investigated the effects of adrenomedullin (AM), which is a multi-functional regulatory peptide, on the production of CXCL10 by HGFs. We revealed that TNF-alpha stimulation induced CXCL10 production by HGFs. HGFs expressed AM and AM receptors, calcitonin-receptor-like receptor (CRLR) and receptor-activity-modifying protein (RAMP) 2, mRNAs constitutively. AM treatment supressed CXCL10 production by TNF-alpha-stimulated HGFs. Moreover, we elucidated that AM produced by HGFs inhibited CXCL10 production by HGFs, because AM antagonist enhanced CXCL10 production by HGFs. TNF-alpha treatment enhanced CRLR and RAMP2 mRNA expression in HGFs. Furthermore, AM is expressed in human periodontal tissues, including both inflamed and clinically healthy tissues. These results suggest that the CXCL10 produced by HGFs may be involved in the migration of leucocytes into inflamed tissues and related to exacerbation of periodontal disease. AM might be a therapeutic target of periodontal disease, because AM can inhibit CXCL10 production by HGFs.
(キーワード): 歯周炎 (periodontal disease)
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2249.2008.03647.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18435806; ● Search Scopus @ Elsevier (PMID): 18435806; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2008.03647.x

(DOI: 10.1111/j.1365-2249.2008.03647.x, PubMed: 18435806) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
CXC chemokine ligand 16 in periodontal diseases: expression in diseased tissues and production by cytokine-stimulated human gingival fibroblasts.,
Clinical and Experimental Immunology, Vol.149, No.1, 146-154, 2007.

(要約): Periodontal disease is an inflammatory disorder characterized by the involvement of chemokines that are important for the recruitment of leucocytes. Several cytokines are involved in regulating levels of chemokines in periodontal disease. CXCL16 is a chemokine related to the migration of T helper 1 (Th1) cells and natural killer (NK) cells. In this study, we examined its expression in periodontal tissues. Moreover, we investigated the effects of cytokines on the production of CXCL16 by human gingival fibroblast (HGF). Reverse transcription-polymerase chain reaction (RT-PCR) analysis and immunohistochemistry revealed that CXCL16 and its receptor, CXCR6, were expressed at the mRNA and protein levels in diseased tissues. Proinflammatory cytokines [interleukin (IL)-1beta, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma] increased the mRNA expression and release of CXCL16 in a dose-dependent manner. Moreover, treatment of HGFs with IFN-gamma in combination with IL-1beta had a synergistic effect on the production of CXCL16. On the other hand, IL-4 and IL-13 inhibited the IL-1beta-induced CXCL16 production by HGFs. Inhibitors of A disintegrin and metalloprotease (ADAM)10 and ADAM17, a recently identified protease of CXCL16, reduced the amount of CXCL16 released from HGFs. These results suggest that the CXCL16 produced by HGFs may be involved in the migration of leucocytes into inflamed tissues, and provide evidence that CXCL16 production is controlled by cytokines in periodontal disease.
(キーワード): Aged / Cells, Cultured / Chemokines, CXC / Chronic Disease / Cytokines / Female / Fibroblasts / Gene Expression / Gingiva / Humans / Interferon-gamma / Interleukin-13 / Interleukin-1beta / Interleukin-4 / Male / Metalloproteases / Middle Aged / Mitogen-Activated Protein Kinases / Periodontitis / RNA, Messenger / Receptors, Chemokine / Receptors, Scavenger / Receptors, Virus / Reverse Transcriptase Polymerase Chain Reaction
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2249.2007.03398.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17459077; ● Search Scopus @ Elsevier (PMID): 17459077; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2007.03398.x

(DOI: 10.1111/j.1365-2249.2007.03398.x, PubMed: 17459077) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Proinflammatory effects of tumour necrosis factor-like weak inducer of apoptosis (TWEAK) on human gingival fibroblasts.,
Clinical and Experimental Immunology, Vol.146, No.3, 540-549, 2006.

(要約): Tumour necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), a member of the TNF family, is a multi-functional cytokine that regulates cellular proliferation, angiogenesis, inflammation and apoptosis. In this study, we investigated TWEAK expression in periodontally diseased tissues and the effect of TWEAK on human gingival fibroblasts (HGF). Reverse transcription-polymerase chain reaction (RT-PCR) analysis and immunohistochemistry revealed that TWEAK and the TWEAK receptor, fibroblast growth factor-inducible 14 (Fn14), mRNA and protein were expressed in periodontally diseased tissues. HGF expressed Fn14 and produced interleukin (IL)-8 and vascular endothelial growth factor (VEGF) production upon TWEAK stimulation in a dose-dependent manner. The IL-8 and VEGF production induced by TWEAK was augmented synergistically by simultaneous stimulation with transforming growth factor (TGF)-beta1 or IL-1beta. IL-1beta and TGF-beta1 enhanced Fn14 expression in a dose-dependent manner. Moreover, TWEAK induced intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression on HGF in a dose-dependent manner. The ICAM-1 expression induced by TWEAK was augmented by TGF-beta1. On the other hand, the TWEAK-induced VCAM-1 expression was inhibited by TGF-beta1. Phosphatidylinositol 3-kinase (PI3K) and nuclear factor-kappaB (NF-kappaB) inhibitor inhibit both ICAM-1 and VCAM-1 expression induced by TWEAK. However, mitogen-activated protein kinase (MEK) and c-Jun NH2-terminal kinase (JNK) inhibitor enhanced only VCAM-1 expression on HGF. These results suggest that TWEAK may be involved in the pathophysiology of periodontal disease. Moreover, in combination with IL-1beta or TGF-beta1, TWEAK may be related to the exacerbation of periodontal disease to induce proinflammatory cytokines and adherent molecules by HGF.
(キーワード): Adult / Aged / Aged, 80 and over / Apoptosis / Cells, Cultured / Dose-Response Relationship, Immunologic / Female / Fibroblasts / Gene Expression / Gingiva / Humans / Intercellular Adhesion Molecule-1 / Interleukin-1beta / Interleukin-8 / Male / Middle Aged / Periodontitis / RNA, Messenger / Receptors, Tumor Necrosis Factor / Reverse Transcriptase Polymerase Chain Reaction / Signal Transduction / Transforming Growth Factor beta1 / Tumor Necrosis Factors / Vascular Cell Adhesion Molecule-1 / Vascular Endothelial Growth Factor A
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2249.2006.03233.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17100776; ● Search Scopus @ Elsevier (PMID): 17100776; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2006.03233.x

(DOI: 10.1111/j.1365-2249.2006.03233.x, PubMed: 17100776) Ikuko Hosokawa, Yoshitaka Hosokawa, H Komatsuzawa, RB Goncalves, N Karimbux, MH Napimoga, Makoto Seki, K Ouhara, M Sugai, Martin A Taubman and Toshihisa Kawai :
Innate immune peptide LL-37 displays distinct expression pattern from beta-defensins in inflamed gingival tissue.,
Clinical and Experimental Immunology, Vol.146, No.2, 218-225, 2006.

(要約): Anti-microbial peptides produced from mucosal epithelium appear to play pivotal roles in the host innate immune defence system in the oral cavity. In particular, human beta-defensins (hBDs) and the cathelicidin-type anti-microbial peptide, LL-37, were reported to kill periodontal disease-associated bacteria. In contrast to well-studied hBDs, little is known about the expression profiles of LL-37 in gingival tissue. In this study, the anti-microbial peptides expressed in gingival tissue were analysed using immunohistochemistry and enxyme-linked immunosorbent assay (ELISA). Immunohistochemistry revealed that neutrophils expressed only LL-37, but not hBD-2 or hBD-3, and that such expression was prominent in the inflammatory lesions when compared to healthy gingivae which showed very few or no LL-37 expressing neutrophils. Gingival epithelial cells (GEC), however, expressed all three examined anti-microbial peptides, irrespective of the presence or absence of inflammation. Moreover, as determined by ELISA, the concentration of LL-37 in the gingival tissue homogenates determined was correlated positively with the depth of the gingival crevice. Stimulation with periodontal bacteria in vitro induced both hBD-2 and LL-37 expressions by GEC, whereas peripheral blood neutrophils produced only LL-37 production, but not hBD-2, in response to the bacterial stimulation. These findings suggest that LL-37 displays distinct expression patterns from those of hBDs in gingival tissue.
(キーワード): Adult / Aged / Antigens, Bacterial / Antimicrobial Cationic Peptides / Bacteria / Cells, Cultured / Enzyme-Linked Immunosorbent Assay / Female / Gene Expression Regulation / Gingiva / Gingivitis / Humans / Immunoenzyme Techniques / Male / Middle Aged / Neutrophils / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction / beta-Defensins
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2249.2006.03200.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17034573; ● Search Scopus @ Elsevier (PMID): 17034573; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2006.03200.x

(DOI: 10.1111/j.1365-2249.2006.03200.x, PubMed: 17034573) Toshihisa Kawai, Takashi Matsuyama, Yoshitaka Hosokawa, Seichou Makihira, Makoto Seki, Karimbux Nadeem, Goncalves B. Reginaldo, Valverde Paloma, Dibart Serge, Li Yi-Ping, Miranda A. Leticia, Ernst W.O. Cory, Izumi Yuichi and Martin A Taubman :
B and T Lymphocytes Are the Primary Sources of RANKL in the Bone Resorptive Lesion of Periodontal Disease,
The American Journal of Pathology, Vol.169, No.3, 987-998, 2006.

(要約): Receptor activator of nuclear factor-kappaB (RANKL)-mediated osteoclastogenesis plays a pivotal role in inflammatory bone resorption. The aim of this study was to identify the cellular source of RANKL in the bone resorptive lesions of periodontal disease. The concentrations of soluble RANKL, but not its decoy receptor osteoprotegerin, measured in diseased tissue homogenates were significantly higher in diseased gingival tissues than in healthy tissues. Double-color confocal microscopic analyses demonstrated less than 20% of both B cells and T cells expressing RANKL in healthy gingival tissues. By contrast, in the abundant mononuclear cells composed of 45% T cells, 50% B cells, and 5% monocytes in diseased gingival tissues, more than 50 and 90% of T cells and B cells, respectively, expressed RANKL. RANKL production by nonlymphoid cells was not distinctly identified. Lymphocytes isolated from gingival tissues of patients induced differentiation of mature osteoclast cells in a RANKL-dependent manner in vitro. However, similarly isolated peripheral blood B and T cells did not induce osteoclast differentiation, unless they were activated in vitro to express RANKL; emphasizing the osteoclastogenic potential of activated RANKL-expressing lymphocytes in periodontal disease tissue. These results suggest that activated T and B cells can be the cellular source of RANKL for bone resorption in periodontal diseased gingival tissue.
(キーワード): B-Lymphocytes / Bone Resorption / Carrier Proteins / Cell Differentiation / Cells, Cultured / Gene Expression Regulation / Gingiva / Glycoproteins / Humans / Lymphocyte Activation / Membrane Glycoproteins / Microscopy, Confocal / Osteoclasts / Osteoprotegerin / Periodontitis / RANK Ligand / Receptor Activator of Nuclear Factor-kappa B / Receptors, Cytoplasmic and Nuclear / Receptors, Tumor Necrosis Factor / T-Lymphocytes
(出版サイトへのリンク): ● Publication site (DOI): 10.2353/ajpath.2006.060180
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16936272; ● Search Scopus @ Elsevier (PMID): 16936272; ● Search Scopus @ Elsevier (DOI): 10.2353/ajpath.2006.060180

(DOI: 10.2353/ajpath.2006.060180, PubMed: 16936272) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Cytokines differentially regulate ICAM-1 and VCAM-1 expression on human gingival fibroblasts.,
Clinical and Experimental Immunology, Vol.144, No.3, 494-502, 2006.

(要約): The expression of intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) on human gingival fibroblasts (HGF) may be important for migration and retention of inflammatory cells in periodontally diseased tissue. This study aimed to assess which cytokines regulate ICAM-1 and VCAM-1 expression on HGF. Tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma enhanced both ICAM-1 and VCAM-1 expression on HGF. Interleukin (IL)-1beta mainly up-regulated ICAM-1 expression. On the other hand, IL-4 and IL-13 enhanced only VCAM-1 expression on HGF. IL-10 did not modulate both ICAM-1 and VCAM-1 expression. Transforming growth factor (TGF)-beta1 enhanced ICAM-1 expression. However, TGF-beta1 inhibited the VCAM-1 expression induced by TNF-alpha or IL-4. Both ICAM-1 and VCAM-1 expression by HGF was inhibited by nuclear factor-kappaB (NF-kappaB) activation inhibitor (MG-132). Mitogen-activated protein kinases (MAPK) inhibitors did not influence ICAM-1 expression induced by TNF-alpha. Interestingly, VCAM-1 expression was enhanced by MEK inhibitor (PD98059) and c-Jun NH2-terminal kinase (JNK) inhibitor (SP600125). These results mean that the balance of cytokines in periodontally diseased tissue may be essential for control of ICAM-1 and VCAM-1 expression on HGF, and the balance of ICAM-1 and VCAM-1 expression might be important for regulation of leucocytes infiltration and retention in periodontally diseased tissue.
(キーワード): Cells, Cultured / Cytokines / Drug Synergism / Enzyme Inhibitors / Fibroblasts / Flow Cytometry / Gene Expression Regulation / Gingiva / Humans / Imidazoles / Intercellular Adhesion Molecule-1 / Leupeptins / Mitogen-Activated Protein Kinase Kinases / NF-kappa B / Pyridines / RNA, Messenger / Recombinant Proteins / Reverse Transcriptase Polymerase Chain Reaction / Vascular Cell Adhesion Molecule-1
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2249.2006.03064.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16734619; ● Search Scopus @ Elsevier (PMID): 16734619; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2006.03064.x

(DOI: 10.1111/j.1365-2249.2006.03064.x, PubMed: 16734619) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Increase of CCL20 expression by human gingival fibroblasts upon stimulation with cytokines and bacterial endotoxin,
Clinical and Experimental Immunology, Vol.142, No.2, 285-291, 2005.

(要約): We have demonstrated recently that CCL20 was expressed in periodontal diseased tissues and abundant CCR6 positive T cells infiltrated in periodontally diseased tissue. However, it is uncertain which cells can elicit CCL20 production. In the present study, we examined the properties of CCL20 production by human gingival fibroblasts (HGF) culture. Here, we report that interleukin-1 beta (IL-1beta), tumour necrosis factor-alpha (TNF-alpha) and Escherichia coli lipopolysaccharide (LPS) can significantly induce the production of CCL20 by HGF. We found that TNF-alpha and E. coli LPS enhanced the production of CCL20 by HGF treated with IL-1beta. In contrast, interferon-gamma (IFN-gamma) dramatically diminished CCL20 production induced by IL-1beta. Moreover, we demonstrated that nuclear factor-kappaB (NF-kappaB), p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinases (ERK) play an important role in mediating the production of CCL20 induced by IL-1beta and TNF-alpha. On the other hand, we found that not only NF-kappaB, p38 MAPK and ERK but also c-Jun NH2-terminal kinase (JNK) are involved in CCL20 production induced by E. coli LPS. Finally, we found that HGF express CCR6, CCL20 receptor, and CCL20 induced vascular endothelial growth factor (VEGF) by HGF. Taken together, these findings that HGF will be a source of CCL20 in periodontal tissue, and the CCL20 production will be controlled by proinflammatory cytokine and bacterial LPS in periodontally diseased tissue. Thus, CCL20 by HGF might be involved in inflammatory cells infiltration, and promote the progression of periodontal disease.
(キーワード): CCL20 / fibroblast / 歯周炎 (periodontal disease)
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2249.2005.02912.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16232215; ● Search Scopus @ Elsevier (PMID): 16232215; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2005.02912.x

(DOI: 10.1111/j.1365-2249.2005.02912.x, PubMed: 16232215) Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae, Keiji Murakami, Yoichiro Miyake and Takashi Matsuo :
CXCL12 and CXCR4 expression by human gingival fibroblasts in periodontal disease,
Clinical and Experimental Immunology, Vol.141, No.3, 467-474, 2005.

(要約): CXCL12 is a CXC chemokine that is related to lymphocyte infiltration and angiogenesis in inflammatory sites such as arthritis. However, the expression and roles of CXCL12 in periodontal disease are uncertain. The aim of this study was to assess the expression of CXCL12 and its receptor, CXCR4, in periodontal tissue and to investigate the properties of CXCL12 and CXCR4 expression by human gingival fibroblasts (HGF). RT-PCR analysis revealed that CXCL12 and CXCR4 mRNA were expressed in both normal gingival tissues and periodontal diseased tissues. Immunohistochemistry disclosed that CXCL12 was expressed and CXCR4 positive cells were found in both normal and periodontal diseased gingival tissues. Our in vitro experiments elucidated that HGF constitutively produced CXCL12, and the levels were enhanced by stimulation with tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), regulated upon activation normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein 3(alpha) (MIP-3(alpha)). On the other hand, heat killed Porphyromonas gingivalis (P. gingivalis) and P. gingivalis LPS reduced the CXCL12 production by HGF. Flow cytometry analysis clarified that CXCR4 was highly expressed on HGF, and CXCR4 expression was abrogated by TNF-alpha, IFN-gamma and P. gingivalis LPS. Moreover, CXCL12 induced vascular endothelial growth factor (VEGF) production by HGF. Our results demonstrated that CXCL12 might be related to CXCR4+ cells infiltration and angiogenesis both in normal periodontal tissues and periodontal diseased tissue. P. gingivalis, a known periodontal pathogen, inhibits the production of CXCL12 and the expression of CXCR4 by HGF. This fact means that P. gingivalis may inhibit CXCR4+ cells infiltration and neovascularization in periodontal tissue and escape from the immune response.
(キーワード): CXCL12 / CXCR4 / fibroblast / 歯周炎 (periodontal disease) / Porphyromonas gingivalis
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2249.2005.02852.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16045736; ● Search Scopus @ Elsevier (PMID): 16045736; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2005.02852.x

(DOI: 10.1111/j.1365-2249.2005.02852.x, PubMed: 16045736) Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Hideaki Nakae and Takashi Matsuo :
Expression of fractalkine (CX3CL1) and its receptor, CX3CR1, in periodontal diseased tissue,
Clinical and Experimental Immunology, Vol.139, No.3, 506-512, 2005.

(要約): The regulatory role of chemokines and chemokine receptors on specific leucocyte recruitment into periodontal diseased tissue is poorly characterized. We observed that leucocytes infiltrating inflamed gingival tissue expressed marked levels of CX3CR1. In periodontal diseased tissue, the expression of fractalkine and CX3CR1 mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) and further, fractalkine was distributed mainly on endothelial cells, as shown by immunohistochemistry. Moreover, we can detect CX3CR1-expressing cells infiltrated in periodontal diseased tissue by immunohistochemical staining. Furthermore, fractalkine production by human umbilical vein endothelial cells (HUVEC) was up-regulated by pathogen-associated molecular patterns (PAMPs), including Porphyromonas gingivalis lipopolysaccharide (LPS). Thus, these findings suggested that CX3CR1 and the corresponding chemokine, fractalkine may have an important regulatory role on specific leucocyte migration into inflamed periodontal tissue.
(キーワード): CX3CR1 / fractalkine / 歯周炎 (periodontal disease)
(出版サイトへのリンク): ● Publication site (DOI): 10.1111/j.1365-2249.2005.02675.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15730397; ● Search Scopus @ Elsevier (PMID): 15730397; ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2005.02675.x

(DOI: 10.1111/j.1365-2249.2005.02675.x, PubMed: 15730397) Tadashi Nakanishi, Kanako Takahashi, Yoshitaka Hosokawa, Tomohiko Adachi, Hideaki Nakae and Takashi Matsuo :
Expression of macrophage inflammatory protein 3alpha in human inflamed dental pulp tissue,
Journal of Endodontics, Vol.31, No.2, 84-87, 2005.

(要約): Severe pulpitis resulting from dental caries is characterized by marked inflammatory infiltrate such as lymphocytes. Little is known about the recruitment of these cells into the dental pulp lesions of carious teeth. Macrophage inflammatory protein-3alpha (MIP-3alpha), a CC chemokine attracts CC chemokine receptor 6 (CCR6)-expressing T cells. We examined the distribution of MIP-3alpha-positive and/or CCR6-positive cells in human inflamed and normal dental pulp by immunohistochemistry. MIP-3alpha was observed in all inflamed pulp sections, and was mostly distributed in macrophages that had accumulated in the area adjacent to carious lesions. Furthermore, CCR6 expression was also observed in the infiltrating lymphocytes. In contrast, MIP-3alpha and CCR6 were rarely detected in normal pulp. These findings suggest that MIP-3alpha plays a role in the advancement of pulpal inflammation via the recruitment of CCR6-expressing lymphocytes.
(キーワード): Adult / Case-Control Studies / Chemokine CCL20 / Chemokines, CC / Chemotaxis, Leukocyte / Dental Caries / Humans / Immunohistochemistry / Macrophage Inflammatory Proteins / Middle Aged / Pulpitis / Receptors, CCR6 / Receptors, Chemokine / T-Lymphocytes
(出版サイトへのリンク): ● Publication site (DOI): 10.1097/01.don.0000143414.22112.57
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15671814; ● Search Scopus @ Elsevier (PMID): 15671814; ● Search Scopus @ Elsevier (DOI): 10.1097/01.don.0000143414.22112.57

(DOI: 10.1097/01.don.0000143414.22112.57, PubMed: 15671814) Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Kanako Takahashi, Hiromichi Yumoto, Kazumi Ozaki and Takashi Matsuo :
Macrophage Inflammatory Protein 3α-CC chemokine receptor 6 interactions play an important role in CD4⁺ T-cell accumulation in periodontal diseased tissue.,
Clinical and Experimental Immunology, Vol.128, No.3, 548-554, 2002.

(要約): The regulatory role of chemokines and chemokine receptors on specific lymphocyte recruitment into periodontal diseased tissue is poorly characterized. We observed that lymphocytes infiltrating inflamed gingival tissue expressed marked levels of CCR6. In periodontal diseased tissue, the expression of MIP-3alpha mRNA was detected by RT-PCR and further, MIP-3alpha was distributed in the basal layer of gingival epithelial cells, microvascular endothelial cells and the areas of inflammatory cells as shown by immunohistochemistry. Moreover, CCR6-expressing cells infiltrated into periodontal diseased tissue, and the proportion of CCR6-positive CD4+ T cells was significantly elevated in periodontal diseased tissue compared with peripheral blood in the same patients. Furthermore, gingival lymphocytes isolated from patients showed migration toward MIP-3alpha in an in vitro chemotaxis assay in which migration was abrogated by specific antibody to CCR6. Thus, these findings suggested that CCR6 and the corresponding chemokine, MIP-3alpha may have an important regulatory role in specific lymphocyte migration into inflamed periodontal tissue.
(キーワード): CCR6 / MIP-3 alpha / periodontal disease / MONOCYTE CHEMOATTRACTANT PROTEIN-1 / INFLAMED HUMAN GINGIVA / IMMUNOHISTOLOGICAL ANALYSIS / SELECTIVE RECRUITMENT / INDUCIBLE EXPRESSION / BACTERIA / IMMUNITY / HEALTHY / LESIONS / SUBSETS
(出版サイトへのリンク): ● Publication site (DOI): 10.1046/j.1365-2249.2002.01865.x
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12067311; ● Search Scopus @ Elsevier (PMID): 12067311; ● Search Scopus @ Elsevier (DOI): 10.1046/j.1365-2249.2002.01865.x

(DOI: 10.1046/j.1365-2249.2002.01865.x, PubMed: 12067311) Tadashi Nakanishi, Hirotoshi Shimizu, Yoshitaka Hosokawa and Takashi Matsuo :
An immunohistological study on cyclooxygenase-2 in human dental pulp.,
Journal of Endodontics, Vol.27, No.6, 385-388, 2001.

(要約): Characteristics of cyclooxygenase-2 (COX-2) expressing cells in human dental pulp were immunohistologically studied. Extirpated pulpal tissues from extracted teeth were examined to elucidate the localization and distribution of COX-2. Pulpal tissues were examined by the labeled streptavidin biotin method using specific mouse monoclonal antibodies for COX-2. Cell types of the COX-2 expressing cells were also investigated by the double stain technique using both monoclonal antibodies for CD68/macrophage and anti-COX-2. COX-2 expressing cells could be found in all of the inflamed pulps, and these cells were mostly distributed close to the area of accumulation of inflammatory cells. COX-2 was mainly expressed in fibroblasts rather than macrophages. In contrast, COX-2 expressing cells were scarcely found in the normal pulps. These findings indicate that pulpal fibroblasts, as well as macrophages, may participate in the production of prostaglandin through COX-2 expression in pulpal inflammation, and might be involved in the pathogenesis of irreversible pulpitis.
(キーワード): Adult / Antibodies, Monoclonal / Antigens, CD / Antigens, Differentiation, Myelomonocytic / Coloring Agents / Cyclooxygenase 2 / Dental Pulp / Fibroblasts / Fluorescent Dyes / Humans / Immunoenzyme Techniques / Immunohistochemistry / Isoenzymes / Macrophages / Membrane Proteins / Middle Aged / Peroxidases / Prostaglandin-Endoperoxide Synthases / Prostaglandins / Pulpitis
(出版サイトへのリンク): ● Publication site (DOI): 10.1097/00004770-200106000-00003
(文献検索サイトへのリンク): ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11487130; ● Search Scopus @ Elsevier (PMID): 11487130; ● Search Scopus @ Elsevier (DOI): 10.1097/00004770-200106000-00003

(DOI: 10.1097/00004770-200106000-00003, PubMed: 11487130)

MISC

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総説・解説

武川大輔, 米倉和秀, 蔵本瞳, 伊田百美香, 細川由樹, 細川育子, 細川義隆, 菅俊行, 中西正, 保坂啓一 :
2級コンポジットレジン修復のキーポイント,
Journal of Oral Health and Biosciences, Vol.36, No.1, 8-12, 2023年9月.

(キーワード): 歯科医療 (dental care)
(徳島大学機関リポジトリ): ● Metadata: 118637
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1050579289345785472

(徳島大学機関リポジトリ: 118637, CiNii: 1050579289345785472) 細川義隆, 細川育子 :
歯周病の発症と進行のメカニズム,
診断と治療, Vol.110, No.9, 1125-1128, 2022年9月.

(キーワード): 歯周組織破壊 / 免疫応答 / 歯肉上皮細胞 / 歯肉線維芽細胞 / 免疫担当細胞 / シシュウソシキハカイ / メンエキオウトウ / シニクジョウヒサイボウ / シニクセンイガサイボウ / メンエキタントウサイボウ
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1520575053166515456

(CiNii: 1520575053166515456) 細川育子, 細川義隆 :
香辛料含有成分を歯周炎治療に用いるための基礎的研究,
地域ケアリング, Vol.23, No.12, 75-78, 2021年11月.

(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1522543656123967488

(CiNii: 1522543656123967488) 細川育子, 細川義隆 :
柑橘類果皮含有生理活性物質を歯周病治療に応用するための基礎的研究,
月刊メディカル・サイエンス・ダイジェスト, Vol.47, No.10, 36-37, 2021年9月. 細川育子, 細川義隆 :
香辛料含有成分を歯周炎治療に用いるための基礎的研究,
アグリバイオ, Vol.5, No.9, 784-788, 2021年8月.

(キーワード): 歯周炎 / カルノシン酸 / 炎症性メディエーター / シシュウエン / カルノシンサン / エンショウセイメディエーター
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1522262181121344768

(CiNii: 1522262181121344768) 細川義隆 :
歯周炎病変局所への白血球浸潤メカニズムの解析ならびに歯周炎治療薬の探索,
日本歯科保存学雑誌, Vol.62, No.6, 260-262, 2020年1月.

(出版サイトへのリンク): ● Publication site (DOI): 10.11471/shikahozon.62.260
(文献検索サイトへのリンク): ● CiNii @ 国立情報学研究所 (CRID): 1390565134815118848; ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.62.260

(DOI: 10.11471/shikahozon.62.260, CiNii: 1390565134815118848) 細川義隆 :
歯周炎病変局所へのリンパ球浸潤機構の解析,
日本歯周病学会会誌, Vol.57, No.2, 61-69, 2015年7月. 細川義隆 :
歯周炎におけるケモカイン発現および発現制御に関する研究,
四国歯学会雑誌, Vol.20, No.2, 235-240, 2008年1月.

(徳島大学機関リポジトリ): ● Metadata: 109768

(徳島大学機関リポジトリ: 109768) 河井敬久, 牧平清超, 細川義隆, 関誠, Taubman A Martin :
歯周病における活性化T細胞およびB細胞の組織破壊への関与,
炎症と免疫, Vol.12, No.4, 425-433, 2004年7月. 細川義隆, 中西正, 松尾敬志 :
歯周炎とケモカイン,
臨床免疫, Vol.38, No.2, 151-156, 2002年2月. 中西正, 高橋加奈子, 細川義隆, 尾崎和美, 松尾敬志 :
歯髄炎の病態形成における細菌侵襲と歯髄反応,
四国歯学会雑誌, Vol.14, No.2, 255-263, 2002年.

(キーワード): 歯髄炎 / う蝕関連細菌 / 免疫担当細胞 / プロスタグランディン / サイトカイン (cytokine)

講演・発表

Shindo Satoru, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki and Takashi Matsuo :
The effect of genipin on dendritic cells activation,
93rd General Session & Exhibition of the IADR, Boston, Mar. 2015. Ikuko Hosokawa, Yoshitaka Hosokawa, Shindo Satoru, Kazumi Ozaki and Takashi Matsuo :
Melatonin inhibits inflammatory mediators productions in human periodontal ligament cells,
93rd General Session & Exhibition of the IADR, Boston, Mar. 2015. Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki and Takashi Matsuo :
IL-4 modulates chemokine productions from IL-1-stimulated human periodontal ligament cells,
93rd General Session & Exhibition of the IADR, Boston, Mar. 2015. Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa and Takashi Matsuo :
The effect of genipin on MMP-1 and MMP-3 expression in IL-1beta-stimulated human periodontal ligament cells,
The 15th Joint Scientific Meeting of JSCD-KACD, Gyeongju, Korea, Nov. 2013. Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hiromichi Yumoto, Hideaki Nakae and Takashi Matsuo :
Pro-inflammatory Roles of NOD2 in Human Gingival Fibroblasts,
The 3rd International Symposium on "Oral Sciences to Improve the Quality of Life", Tokushima, Sep. 2008. Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hiromichi Yumoto, Hideaki Nakae and Takashi Matsuo :
Pro-inflammatory Roles of NOD2 in Human Gingival Fibroblasts,
86th General Session and Exhibition of the International Association for Dental Research, Toronto, Jul. 2008. Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Th17 cytokines enhance CCL20 production by human gingival fibroblasts.,
86th General Session and Exhibition of the International Association for Dental Research, Toronto, Jun. 2008. Kayo Mukai, Tadashi Nakanishi, Yoshitaka Hosokawa, Kanako Takahashi and Takashi Matsuo :
Inhibitory effects of catechins on inflammatory reactions in pulp fibroblasts,
84th General Session & Exhibition of the IADR, Brisbane, Jun. 2006. Ikuko Hosokawa, Yoshitaka Hosokawa, RB Goncalves, Martin A Taubman, NY Karimbux, Komatsuzawa Hitoshi and Toshihisa Kawai :
Expressinon of Antibacterial Peptides in Periodontal Disease,
82nd General Session and Exhibition of International Association for Dental Research, Honolulu, Mar. 2004. Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Hiromichi Yumoto and Takashi Matsuo :
LARC-CCR6 Interactions play an important role in CD4+ T cell accumulation in periodontal diseased tissue,
80th General Session and Exhibition of the International Association for Dental Research, San Diego(USA), Mar. 2002. Tadashi Nakanishi, Kanako Takahashi, Yoshitaka Hosokawa, Daisuke Yamaguchi, Chihiro Shinohara, Hiromichi Yumoto and Takashi Matsuo :
Expression of macrophage inflammatory protein-3 α in human pulpitis,
80th General SEssion ofthe IADR(International Association of Dental Research), San Diego(USA), Mar. 2002. Hiromichi Yumoto, Daisuke Yamaguchi, Yoshitaka Hosokawa, Chihiro Shinohara, Tadashi Nakanishi, Hirotoshi Shimizu, Masayoshi Yamada, Hideaki Nakae and Takashi Matsuo :
Expression of IL-18 and IL-18 receptor in human periodontally diseased tissue,
Modern Periodontology New Directions in 21st Century-, Kanagawa(Japan), Jun. 2001. 岡本梨沙, 細川義隆, 細川育子, 下山真弘, 尾崎和美, 保坂啓一 :
TNF-αで刺激されたヒト歯根膜由来細胞の炎症性メディエーター発現に与えるcardamoninの影響,
日本歯科保存学会2023年度秋季学術大会(第159回), 2023年11月. 三枝克啓, 中西正, 蔵本瞳, 細川義隆, 細川育子, 武川大輔, 保坂啓一 :
Sudachitinがヒト歯髄細胞の炎症メディエーター発現に与える影響,
日本歯科保存学会 2023年度春季学術大会(第158回), 2023年6月. 下山真弘, 細川義隆, 細川育子, 保坂啓一 :
TNF-αで刺激されたヒト口腔上皮細胞の炎症性メディエーター産生ならびに抗酸化タンパク質発現に対するErucinの影響,
日本歯科保存学会 2023年度春季学術大会(第158回), 2023年6月. 藤井亜祐美, 嘉手納公威, 佐藤朱里, 下山真弘, 細川育子, 細川義隆 :
イベリンがヒト口腔上皮細胞の炎症性メディエーター産生に及ぼす影響の解析,
第64回歯科基礎医学会学術大会, 2022年9月. 下山真弘, 細川義隆, 細川育子, 保坂啓一 :
6-MSITCはTNF-αが誘導するヒト口腔上皮由来細胞のIL-6およびCXCL10産生を抑制する,
日本歯科保存学会 2022年度春季学術大会(156回), 2022年6月. 細川義隆, 細川育子, 尾崎和美 :
Nobiletinはヒト歯根膜由来細胞のIL-1β誘導炎症性メディエーター産生を抑制する,
2021年度日本歯科保存学会春季学術大会(第154回), 2021年6月. 細川育子, 細川義隆, 尾崎和美 :
Carnosic Acidはヒト歯根膜由来細胞のIL-1β誘導炎症性サイトカイン産生を抑制する,
日本歯科保存学会2020年度春季学術大会, 2020年6月. 細川義隆, 細川育子, 尾崎和美 :
Sudachitinはヒト歯根膜由来細胞のIL-1β誘導炎症性メディエーター産生を抑制する,
日本歯科保存学会2020年度春季学術大会, 2020年6月. 細川育子, 細川義隆, 尾崎和美, 松尾敬志 :
Carnosic acidはヒト口腔上皮細胞のIL-27誘導CXCR3リガンド産生を抑制する,
日本歯科保存学会2018年度秋季学術大会, 2018年11月. 細川義隆, 細川育子, 尾崎和美, 松尾敬志 :
IL-27はヒト口腔上皮細胞のCXCR3リガンド産生を誘導する,
第61回日本歯周病学会春季学術大会, 2018年6月. 細川義隆, 細川育子, 尾崎和美, 松尾敬志 :
IL-29はTNF-αが誘導するヒト口腔上皮細胞のCXCL10産生を増強する,
第60回日本歯周病学会秋季学術大会, 2017年12月. 細川義隆, 細川育子, 尾崎和美, 松尾敬志 :
IL-29はヒト口腔上皮細胞のCXCL10産生を増強する,
第60回日本歯周病学会春季学術大会, 2017年10月. 進藤智, 池田淳史, 細川義隆, 細川育子, 尾崎和美, 松尾敬志 :
シトルリン化ビメンチンは破骨細胞分化を促進する,
日本歯科保存学会2016年度秋季学術大会, 2016年10月. 細川義隆, 細川育子, 進藤智, 尾崎和美, 松尾敬志 :
Gomisin Nはヒト歯根膜由来細胞の炎症性サイトカイン産生を抑制する,
日本歯科保存学会2016年度秋季学術大会, 2016年10月. 細川義隆, 細川育子, 進藤智, 尾崎和美, 松尾敬志 :
Alkanninはヒト歯根膜由来細胞のIL-6およびCCL20産生を抑制する,
第59回春季日本歯周病学会学術大会, 2016年5月. 細川義隆, 細川育子, 進藤智, 尾崎和美, 松尾敬志 :
Alkanninはヒト歯根膜由来細胞のCCR5 ligand産生を誘導する,
日本歯科保存学会2015年度秋季学術大会, 2015年11月. 細川義隆, 細川育子, 進藤智, 尾崎和美, 松尾敬志 :
IL-4がヒト歯根膜由来細胞のCCL11およびCCL20産生に及ぼす影響,
第58回秋季日本歯周病学会学術大会, 2015年9月. 細川義隆 :
歯周炎病変局所へのリンパ球浸潤機構の解析,
第58回春季日本歯周病学会学術大会, 2015年5月. 進藤智, 細川義隆, 細川育子, 尾崎和美, 松尾敬志 :
Shikoninがヒト歯根膜由来細胞のIL-6およびIL-8産生に与える影響,
第141回日本歯科保存学会秋季学術大会, 2014年10月. 進藤智, 細川義隆, 細川育子, 尾崎和美, 松尾敬志 :
GenipinはE.coli LPSが誘導するヒト歯根膜細胞のIL-6およびIL-8産生を抑制する,
第140回日本歯科保存学会春季学術大会, 2014年6月. 細川義隆, 細川育子, 進藤智, 尾崎和美, 松尾敬志 :
活性型ビタミンDはIL-1β刺激ヒト歯根膜細胞の炎症性サイトカイン産生を抑制する,
第140回日本歯科保存学会春季学術大会, 2014年6月. 北中祐太郎, 細川義隆, 細川育子, 進藤智, 尾崎和美, 松尾敬志 :
genipinはTNF-αが誘導するヒト歯根膜由来細胞のIL-6産生を抑制する,
第57回春季歯周病学会学術大会, 2014年5月. 進藤智, 細川義隆, 細川育子, 尾崎和美, 松尾敬志 :
GenipinはIL-1betaが誘導するヒト歯根膜細胞のCCL20およびIL-6 産生を抑制する,
第139回日本歯科保存学会秋季学術大会, 2013年10月. 進藤智, 細川義隆, 細川育子, 尾崎和美, 松尾敬志 :
GenipinはIL-1betaが誘導するヒト歯根膜細胞のCCL20およびIL-6産生を抑制する,
日本歯科保存学雑誌, 70, 2013年10月. 細川義隆, 細川育子, 進藤智, 尾崎和美, 松尾敬志 :
IL-6はIL-1βが誘導するヒト歯根膜由来細胞のCCL20産生を増強する,
日本歯周病学会会誌, 97, 2013年5月. 細川育子, 細川義隆, 尾崎和美, 松尾敬志 :
Adrenomedullinが樹状細胞のTh17関連サイトカイン産生に関与するcell signalingに及ぼす影響,
日本歯科保存学雑誌, 2012年11月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
IL-17AはTNF-aが誘導するヒト歯肉線維芽細胞のCCL20産生を増強する,
日本歯科保存学雑誌, 2012年11月. 石川真琴, 吉田賀弥, 藤原奈津美, 細川義隆, 細川育子, 尾崎和美 :
歯周病原性細菌Porphyromonas gingivalis感染が肝臓糖代謝に及ぼす影響,
日本歯科保存学雑誌, 155, 2012年11月. 細川義隆, 細川育子, 尾崎和美, 中西正, 中江英明, 松尾敬志 :
TNF-alphaとIL-4刺激が誘導するヒト歯肉線維芽細胞のCCL11産生に及ぼす緑茶カテキンの影響,
日本歯科保存学雑誌, 2012年6月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
IL-22はIL-1betaが誘導するヒト歯肉線維芽細胞のCCL20産生を増強する,
日本歯周病学会会誌, 2012年5月. 細川義隆, 細川育子, 尾崎和美, 中西正, 松尾敬志 :
TWEAKがヒト歯肉線維芽細胞のIL-1beta誘導CCL20産生に与える影響,
日本歯科保存学雑誌, 2011年10月. 細川義隆, 細川育子, 尾崎和美, 中西正, 中江英明, 松尾敬志 :
TheaflavinがTNFSF14刺激ヒト歯肉線維芽細胞のIL-6産生に与える影響,
日本歯科保存学雑誌, 2011年6月. 尾崎和美, 藤原奈津美, 石川真琴, 細川育子, 細川義隆, 湯本浩通 :
う蝕関連細菌の家族内伝播と生活習慣による影響に関する研究 ―兄弟姉妹間の差異について―,
134回日本歯科保存学会春季学術大会, 2011年6月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
TLR3 ligandがヒト歯肉線維芽細胞のIL-1beta誘導CCL20産生に与える影響,
日本歯周病学会会誌, 2011年5月. 進藤智, 細川義隆, 細川育子, 尾崎和美, 中西正, 中江英明, 松尾敬志 :
Oncostatin Mが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす紅茶ポリフェノールの影響,
日本歯周病学会会誌, 2011年5月. 細川義隆, 細川育子, 尾崎和美, 中西正, 中江英明, 松尾敬志 :
CatechinがTNFSF14刺激ヒト歯肉線維芽細胞のIL-6産生に与える影響,
日本歯科保存学雑誌, 2010年10月. 橋本玲奈, 細川義隆, 細川育子, 尾崎和美, 中西正, 中江英明, 松尾敬志 :
IL-1betaが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす緑茶カテキンの影響,
日本歯周病学会会誌, 2010年9月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
IL-17AはIL-1betaが誘導するヒト歯肉線維芽細胞のCCL20産生を増強する,
日本歯周病学会会誌, 2010年5月. Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo :
Adrenomedullin inhibits CXCL10 production by human gingival fibroblasts,
56th Annual Meeting of Japanese Association for Dental Research, Nov. 2008. 細川育子, 細川義隆, 尾崎和美, 中江英明, 松尾敬志 :
Toll-like Receptor Ligands刺激が誘導する単球のCCL20産生に及ぼすAdrenomedullinの影響,
第128回日本歯科保存学会秋季学術大会, 2008年11月. 細川育子, 細川義隆, 尾崎和美, 中江英明, 松尾敬志 :
ヒト歯肉線維芽細胞におけるTLR4 ligandが誘導するCXCL10産生に及ぼすAdrenomedullinの影響,
第51回日本歯周病学会秋季学術大会, 2008年10月. 細川育子, 細川義隆, 尾崎和美, 中江英明, 松尾敬志 :
Toll-like Receptor Ligands刺激が誘導する単球のIL-1beta産生に及ぼすAdrenomedullinの影響,
第128回日本歯科保存学会春季学術大会, 2008年6月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
Flagellinがヒト歯肉線維芽細胞のサイトカイン産生および接着分子発現に与える影響,
第128回日本歯科保存学会春季学術大会, 2008年6月. 細川育子, 細川義隆, 尾崎和美, 中江英明, 松尾敬志 :
Adrenomedullinがヒト歯肉線維芽細胞のToll-like Receptor Ligands誘導サイトカイン産生に与える影響,
第51回日本歯周病学会春季学術大会, 2008年4月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
Toll-like receptor ligandsがヒト歯肉線維芽細胞のCXCL10産生に与える影響,
第51回日本歯周病学会春季学術大会, 2008年4月. 細川育子, 細川義隆, 尾崎和美, 中江英明, 松尾敬志 :
Adrenomedulinがヒト歯肉線維芽細胞のサイトカイン産生に与える影響の解析,
第127回日本歯科保存学会秋季学術大会, 2007年11月. Ikuko Hosokawa, Yoshitaka Hosokawa, Kazumi Ozaki, Hiromichi Yumoto, Hideaki Nakae and Takashi Matsuo :
Proinflammatory Roles of NOD2 in Human Gingival Fibroblasts,
第55回国際歯科研究学会日本部会(JADR)総会・学術大会, Nov. 2007. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
サイトカインがヒト歯肉線維芽細胞のCXCL10産生に与える影響,
日本歯周病学会50周年記念学術大会, 2007年9月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
ヒト歯肉線維芽細胞におけるCCL17産生の解析,
第50回春季日本歯周病学会学術大会, 2007年5月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
サイトカイン刺激によるヒト歯肉線維芽細胞におけるCXCL16産生の解析,
第36回日本免疫学会総会・学術集会, 2006年12月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
サイトカインがヒト歯肉線維芽細胞上のICAM-1およびVCAM-1発現に与える影響,
第49回秋季日本歯周病学会学術大会, 2006年10月. 向井佳代, 中西正, 細川義隆, 高橋加奈子, 松尾敬志 :
カテキンが歯髄由来線維芽細胞の炎症性サイトカインおよび接着分子の発現誘導に与える影響,
第27回日本歯内療法学会学術大会, 2006年7月. 向井佳代, 中西正, 細川義隆, 高橋加奈子, 足立智彦, 松尾敬志 :
カテキンが歯髄由来線維芽細胞の炎症性サイトカインおよび接着分子の発現誘導に与える影響,
第124回日本歯科保存学会春季学術大会, 2006年5月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
TWEAKがヒト歯肉線維芽細胞における炎症性サイトカイン産生ならびに接着分子発現に与える影響の解析,
第49回春季日本歯周病学会学術大会, 2006年4月. 細川義隆, 細川育子, 中江英明, 尾崎和美, 松尾敬志 :
炎症性サイトカインおよびLPSはヒト歯肉線維芽細胞のCCL20産生を誘導する,
第48回秋季日本歯周病学会学術大会, 2005年9月. 細川育子, 細川義隆, 尾崎和美, 松尾敬志 :
Langerhans細胞における抗菌ペプチドの発現について,
第48回秋季日本歯周病学会学術大会, 2005年9月. 向井佳代, 中西正, 細川義隆, 高橋加奈子, 足立智彦, 松尾敬志 :
Toll-like receptor リガンドによる歯髄由来繊維芽細胞のIL-8, VEGF, 接着分子発現誘導,
第122回春季日本歯科保存学会, 2005年6月. 向井佳代, 中西正, 細川義隆, 高橋加奈子, 足立智彦, 松尾敬志 :
Toll-like receptor リガンドによる歯髄線維芽細胞のIL-8，VEGF，接着分子の発現誘導,
第122回日本歯科保存学会春季学術大会, 2005年6月. 細川義隆, 細川育子, 尾崎和美, 中江英明, 松尾敬志 :
ヒト歯肉線維芽細胞におけるCXCL12産生ならびに機能的解析,
第47回秋季日本歯周病学会学術大会, 2004年10月. 高橋加奈子, 中西正, 山口大輔, 細川義隆, 湯本浩通, 尾崎和美, 中江英明, 松尾敬志 :
歯髄炎の病態形成におけるLARCおよびCCR6の役割,
第32回日本免疫学会, 2002年12月. 山口大輔, 細川義隆, 篠原千尋, 湯本浩通, 中西正, 中江英明, 松尾敬志 :
歯周炎病変局所におけるFractalkineおよびCX3CR1の発現,
第45回春季日本歯周病学会, 2002年4月. 細川義隆, 中西正, 山口大輔, 清水洋利, 尾崎和美, 中江英明, 松尾敬志 :
歯周炎病変局所におけるLARCおよびCCR6の発現,
第31回日本免疫学会, 2001年12月. 山口大輔, 細川義隆, 湯本浩通, 中西正, 中江英明, 松尾敬志 :
歯周炎病変局所におけるIL-18とその機能に関連する分子の発現について,
第31回日本免疫学会学術集会, 2001年12月. 高橋加奈子, 中西正, 細川義隆, 篠原千尋, 湯本浩通, 尾崎和美, 松尾敬志 :
炎症歯髄におけるLARCおよびCCR6の発現,
第115回秋季日本歯科保存学会, 2001年11月. 細川義隆, 中西正, 山口大輔, 清水洋利, 湯本浩通, 尾崎和美, 松尾敬志 :
歯周炎病変局所におけるLARCおよびCCR6の発現,
第44回秋季日本歯周病学会学術大会, 2001年10月. 山口大輔, 細川義隆, 清水洋利, 篠原千尋, 湯本浩通, 中西正, 松尾敬志 :
歯周炎の病変局所におけるIL-18およびIL-18レセプターの発現,
第44回春季日本歯周病学会学術大会, 2001年4月. 細川義隆, 山口大輔, 清水洋利, 中西正, 尾崎和美, 中江英明, 松尾敬志 :
歯周炎の病巣局所におけるケモカインおよびケモカイン受容体の発現,
第30回日本免疫学会総会, 2000年11月. 清水洋利, 細川義隆, 山口大輔, 中西正, 尾崎和美, 中江英明, 松尾敬志 :
歯周炎の病巣局所におけるリンパ球浸潤に対するケモカインの関与,
第29回日本免疫学会総会, 1999年12月. 清水洋利, 細川義隆, 中西正, 尾崎和美, 中江英明 :
歯周炎の病巣局所におけるVCAM-1,VLA-4を介する接着系の解析,
第28回日本免疫学会, 1998年12月.

研究会・報告書: 研究者総覧に該当データはありませんでした。

特許: 研究者総覧に該当データはありませんでした。
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補助金・競争的資金: ワサビ含有成分を歯周炎治療に用いるための基礎的研究～抗炎症作用に着目して～ (研究課題/領域番号: 22K09984 )
ポリフェノール内包キトサンナノカプセルを用いた口腔バイオフィルム抑制技術の開発 (研究課題/領域番号: 22K09967 )
乳酸菌由来細胞外小胞を用いた歯周病治療戦略ーM1/M2マクロファージに着目してー (研究課題/領域番号: 22K09966 )
柑橘類果皮含有生理活性物質を歯周炎治療に用いるための基礎的研究 (研究課題/領域番号: 19K10151 )
口腔バイオフィルムの分散能と抗菌能を有する光触媒・ポリフェノール合剤の新規開発 (研究課題/領域番号: 19K10132 )
香辛料含有成分を歯周炎治療に用いるための基礎的研究-ローズマリーに着目して- (研究課題/領域番号: 18K09600 )
歯周炎病変局所における炎症性骨吸収に関与する白血球浸潤機構の解析 (研究課題/領域番号: 16K11834 )
ポリフェノール・銀ナノ粒子複合体を応用した口腔バイオフィルム形成制御技術の開発 (研究課題/領域番号: 16K11554 )
歯周病におけるメラトニンの役割解明および治療への応用 (研究課題/領域番号: 15K11392 )
歯髄炎における炎症・抗炎症バランス制御機構の解析とTh17細胞の役割 (研究課題/領域番号: 15K11115 )
歯周炎病変局所におけるTh17細胞浸潤・活性化機構の解析 (研究課題/領域番号: 25463219 )
オートインデューサーの分解を機作とした口腔バイオフィルム形成制御に関する研究 (研究課題/領域番号: 25462962 )
歯髄炎の病態形成における炎症－抗炎症バランス制御の解析 (研究課題/領域番号: 24592871 )
歯周炎病変局所への Th17細胞浸潤機構の解析 (研究課題/領域番号: 23792479 )
アドレノメデュリンの抗菌作用による口腔バイオフィルムの形成抑制効果に関する研究 (研究課題/領域番号: 22592122 )
歯周炎におけるTh17細胞の浸潤・活性化機構の解析 (研究課題/領域番号: 21792123 )
根面齲蝕の病態・病因の解析に基づく新しい診断法と治療法の開発 (研究課題/領域番号: 20592229 )
歯髄保存療法への緑茶カテキン応用に関する研究 (研究課題/領域番号: 20592228 )
ケモカインからみた歯周炎病変局所浸潤リンパ球の組織破壊への関与に関する研究 (研究課題/領域番号: 19791616 )
ケモカインからみた歯周組織破壊におけるリンパ球浸潤メカニズムの解析 (研究課題/領域番号: 17791556 )
象牙細管侵入細菌の菌体内多糖合成に関する動的解析 (研究課題/領域番号: 17591993 )
歯髄炎の病態形成におけるリンパ球浸潤機構と歯髄線維芽細胞の役割に関する研究 (研究課題/領域番号: 16591915 )
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専門分野・研究分野: 歯周炎
所属学会・所属協会: 日本歯周病学会
日本免疫学会
国際歯科研究学会
四国歯学会
日本歯科保存学会
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受賞: 2004年5月, 日本歯周病学会奨励賞 (日本歯周病学会)
2007年2月, 西野瑞穂歯科臨床医学奨励賞 (歯学部)
2008年6月, 日本歯科保存学会奨励賞 (日本歯科保存学会)
2014年10月, 日本歯周病学会学術賞 (日本歯周病学会)
2019年6月, 日本歯科保存学会学術賞 (日本歯科保存学会)
活動: 徳島大学病院医学系研究倫理審査委員会2号委員 (2018年4月〜2022年3月)

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Jグローバル最終確認日: 2024/5/4 01:04
氏名（漢字）: 細川義隆
氏名（フリガナ）: ホソカワヨシタカ
氏名（英字）: Hosokawa Yoshitaka
所属機関: 徳島大学講師

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researchmap最終確認日: 2024/4/28 01:56
氏名（漢字）: 細川義隆
氏名（フリガナ）: ホソカワヨシタカ
氏名（英字）: Hosokawa Yoshitaka
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所属ID: 0344003000
所属: 徳島大学
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2024年5月4日更新

研究者番号: 90346601

所属（現在）: 2024/4/1 : 徳島大学, 病院, 講師

所属（過去の研究課題 情報に基づく）*注記: 2017/4/1 – 2022/4/1 : 徳島大学, 病院, 講師
2016/4/1 : 徳島大学, 大学院医歯薬学研究部(歯学系), 助教
2015/4/1 : 徳島大学, 大学院医歯薬学研究部, 助教
2014/4/1 : 徳島大学, 大学院ヘルスバイオサイエンス研究部, 助教
2011/4/1 – 2014/4/1 : 徳島大学, ヘルスバイオサイエンス研究部, 助教
2012/4/1 : 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教
2007/4/1 – 2012/4/1 : 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教
2006/4/1 : 徳島大学, 大学院ヘルスバイオサイエンス研究部, 助手
2006/4/1 : 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助手
2004/4/1 – 2005/4/1 : 徳島大学, 医学部・歯学部附属病院, 助手

審査区分/研究分野

研究代表者

生物系 / 医歯薬学 / 歯学 / 歯周治療系歯学
小区分57030:保存治療系歯学関連

研究代表者以外

生物系 / 医歯薬学 / 歯学 / 保存治療系歯学
生物系 / 医歯薬学 / 歯学 / 歯周治療系歯学
小区分57030:保存治療系歯学関連

キーワード

研究代表者

歯周炎 / 歯肉線維芽細胞 / サイトカイン / TWEAK / Fn14 / ケモカイン / リンパ球 / Th1細胞 / CXCL16 / 線維芽細胞 / シグナル伝達 / サイト力イン / 線稚芽細胞 / Th17 / Th17細胞 / CCL20 / カテキン / Th１７細胞 / Ｔｈ１７細胞 / IL-6 / IL-22 / 歯根膜由来細胞 / ヒト歯根膜由来細胞 / CXCL10 / 歯根膜細胞 / ＣＣＬ２０ / 白血球 / 歯周組織構成細胞 / CCL11 / STAT6 / IL-29 / 口腔上皮細胞 / CCR5 / CCL3 / CCL5 / Alkannin / NF-κB / 歯学 / 細胞・組織 / 免疫学 / 柑橘類果皮 / 生理活性物質 / 抗炎症作用 / ノビレチン / スダチチン / 炎症性メディエーター / MMP / Akt / 柑橘類果皮含有生理活性物質 / ワサビ / 6-MSITC / シグナル伝達経路

研究代表者以外

カテキン / 歯髄炎 / 歯髄細胞 / 抗炎症作用 / サイトカイン / ケモカイン / シグナル伝達経路 / 根面齲蝕 / ミュータンス菌 / 再石灰化 / 象牙細管侵入細菌 / 歯髄応答 / 自然免疫 / 病原体特異的分子パターン / パターン認識受容体 / 茶カテキン / 自然免疫機構 / バイオフィルム / アドレノメデュリン / 抗菌ペプチド / 歯髄 / 炎症 / 象牙芽細胞 / リンパ球 / クオラムセンシング / オートインデューサー / 細菌関連物質 / 線維芽細胞 / 歯周炎 / 細菌由来物質 / 接着分子 / 白血球 / pulpitis / chemokine / cytokine / bacteria-related products / fibroblast / periodontal disease / 象牙質齲蝕 / Streptococcus mutans / 菌体内多糖 / Quorum Sensing System / Dentinal caries / Intracellular polysaccharide / Quorum sensing system / Th17 / IL-17 / メラトニン / MMP-1 / CXCL10 / IL-27 / TNF-α / MMP / 銀ナノ粒子 / ポリフェノール / Carnosic acid / Rosmarinic acid / ローズマリー / 二酸化チタン / チタニアナノチューブ / 光触媒 / 細胞外小胞 / M１/M２マクロファージ / ナノカプセル / キトサン

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細川 義隆

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細川義隆