Black tea polyphenol inhibits CXCL10 production in oncostatin M-stimulated human gingival fibroblasts

被引：15

作者：

Hosokawa, Yoshitaka ^{[1
]}

Hosokawa, Ikuko ^{[1
]}

Shindo, Satoru ^{[1
]}

Ozaki, Kazumi ^{[2
]}

Nakanishi, Tadashi ^{[1
]}

Nakae, Hideaki ^{[1
]}

Matsuo, Takashi ^{[1
]}

机构：

[1] Univ Tokushima, Grad Sch, Inst Hlth Biosci, Dept Conservat Dent, Tokushima 7708504, Japan

[2] Univ Tokushima, Grad Sch, Inst Hlth Biosci, Dept Oral Hlth Care Promot, Tokushima 7708504, Japan

来源：

INTERNATIONAL IMMUNOPHARMACOLOGY | 2011年 / 11卷 / 06期

关键词：

Theaflavin; CXCL10; Oncostatin M; Fibroblasts; PERIODONTAL-DISEASE; BONE-RESORPTION; EXPRESSION; RECEPTOR; CHEMOKINES; IL-6; THEAFLAVIN-3,3'-DIGALLATE; INTERLEUKIN-11; NEUTROPHILS; PROTEIN-1;

D O I：

10.1016/j.intimp.2011.01.009

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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) beta expression on HGFs. These data provide a novel mechanism where the black tea flavonoid, theaflavin, could provide direct benefits in periodontal disease. (C) 2011 Elsevier B.V. All rights reserved.

引用

页码：670 / 674

页数：5

共 33 条

[1] Epigallocatechin-3-O-gallate inhibits TNFα-induced monocyte chemotactic protein-1 production from vascular endothelial cells [J].

Ahn, Hee Yul ;

Xu, Yi ;

Davidge, Sandra T. .

LIFE SCIENCES, 2008, 82 (17-18) :964-968

[2]

AKIRA K, 2008, AM J HUM GENET, V82, P73

[3]

BROWN TJ, 1987, J IMMUNOL, V139, P2977

[4]

FUJIHASHI K, 1993, J PERIODONTOL, V64, P400

[5] Patterns of chemokines and chemokine receptors expression in different forms of human periodontal disease [J].

Garlet, GP ;

Martins, W ;

Ferreira, BR ;

Milanezi, CM ;

Silva, JS .

JOURNAL OF PERIODONTAL RESEARCH, 2003, 38 (02) :210-217

[6] Chemokines in human periodontal disease tissues [J].

Gemmell, E ;

Carter, CL ;

Seymour, GJ .

CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2001, 125 (01) :134-141

[7] Oncostatin M production by blood and alveolar neutrophils during acute lung injury [J].

Grenier, A ;

Combaux, D ;

Chastre, J ;

Gougerot-Pocidalo, MA ;

Gibert, C ;

Dehoux, M ;

Chollet-Martin, S .

LABORATORY INVESTIGATION, 2001, 81 (02) :133-141

[8]

GROVE RI, 1991, J LIPID RES, V32, P1889

[9] Expression of fractalkine (CX3CL1) and its receptor, CX3CR1, in periodontal diseased tissue [J].

Hosokawa, Y ;

Nakanishi, T ;

Yamaguchi, D ;

Nakae, H ;

Matsuo, T .

CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2005, 139 (03) :506-512

[10] Macrophage Inflammatory Protein 3α-CC chemokine receptor 6 interactions play an important role in CD4+ T-cell accumulation in periodontal diseased tissue [J].

Hosokawa, Y ;

Nakanishi, T ;

Yamaguchi, D ;

Takahashi, K ;

Yumoto, H ;

Ozaki, K ;

Matsuo, T .

CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2002, 128 (03) :548-554

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