Abstract
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.
Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Catechin / analogs & derivatives*
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Catechin / pharmacology
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Down-Regulation / drug effects
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Enzyme Activation / drug effects
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Flavonoids / pharmacology
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Inflammation Mediators / metabolism
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Intracellular Signaling Peptides and Proteins / metabolism*
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MAP Kinase Signaling System / drug effects
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Macrophages, Peritoneal / drug effects
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Macrophages, Peritoneal / metabolism
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Mice
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Molecular Weight
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Peptidoglycan / pharmacology*
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Phenols / pharmacology
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Polyphenols
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Receptors, Laminin / metabolism*
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Signal Transduction / drug effects*
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Tea / chemistry*
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Toll-Like Receptor 2 / metabolism*
Substances
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Flavonoids
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Inflammation Mediators
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Intracellular Signaling Peptides and Proteins
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Peptidoglycan
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Phenols
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Polyphenols
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Receptors, Laminin
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Tea
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Tlr2 protein, mouse
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Toll-Like Receptor 2
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Tollip protein, mouse
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Catechin
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epigallocatechin gallate