Green tea polyphenol epigallocatechin-3-gallate inhibits TLR2 signaling induced by peptidoglycan through the polyphenol sensing molecule 67-kDa laminin receptor

被引:68
作者
Byun, Eui-Hong [1 ,4 ,5 ]
Omura, Toshinori [1 ]
Yamada, Koji [1 ]
Tachibana, Hirofumi [1 ,2 ,3 ]
机构
[1] Kyushu Univ, Dept Biosci & Biotechnol, Fac Agr, Fukuoka 8128581, Japan
[2] Kyushu Univ, Dept Funct Metab Design, Bioarchitecture Ctr, Higashi Ku, Fukuoka 8128581, Japan
[3] Kyushu Univ, Innovat Ctr Med Redox Nav, Higashi Ku, Fukuoka 8128582, Japan
[4] Chungnam Natl Univ, Dept Microbiol, Taejon 301747, South Korea
[5] Chungnam Natl Univ, Res Inst Med Sci, Coll Med, Taejon 301747, South Korea
基金
日本学术振兴会;
关键词
Epigallocatechin-3-gallate; 67-kDa laminin receptor; Peptidoglycan; Toll-like receptor 2; Toll-interacting protein; FC-EPSILON-RI; BACTERIAL PEPTIDOGLYCAN; STAPHYLOCOCCUS-AUREUS; NEGATIVE REGULATION; KAPPA-B; EXPRESSION; PATHWAY; LIPOPOLYSACCHARIDE; TRANSCRIPTION; TOLLIP;
D O I
10.1016/j.febslet.2011.02.010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Here we show the molecular basis for the inhibition of peptidoglycan (PGN)-induced TLR2 signaling by a major green tea polyphenol epigallocatechin-3-gallate (EGCG). Recently, we identified the 67-kDa laminin receptor (67LR) as the cell-surface EGCG receptor. Anti-67LR antibody treatment or silencing of 67LR resulted in abrogation of the inhibitory action of EGCG on PGN-induced production of pro-inflammatory mediators and activation of mitogen-activated protein kinases. Silencing of Toll-interacting protein (Tollip), a negative regulator of TLR signaling impaired the TLR2 signaling inhibitory activity of EGCG, suggesting that TLR2 response could be inhibited by EGCG via 67LR and Tollip. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:814 / 820
页数:7
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