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pubmed-article:19426837pubmed:abstractTextAlthough green tea polyphenol catechin is considered as a potential anti-inflammatory agent, its effect on bacterial component-induced inflammation has been poorly investigated. We examined the capacity of epigallocatechin gallate (EGCG) to regulate leukocyte responses to bacterial chemotactic peptide N-formylmethionyl-leucyl-phenylalanine (fMLF), which is recognized by a human G protein-coupled receptor FPR on phagocytic leukocytes. Pretreatment of human monocytic cells or FPR-transfected rat basophilic leukemia cells (ETFR cells) with EGCG significantly inhibited fMLF-induced chemotaxis. Intraperitoneal administration of EGCG in mice suppressed fMLF-induced leukocyte infiltration into the air pouch created in the skin. Mechanistic studies revealed that EGCG dose-dependently suppressed fMLF-induced calcium flux in monocytic cells and ETFR cells. fMLF-induced ETFR cell migration was significantly inhibited by a specific MEK1/2 inhibitor, PD98059, which was associated with reduction in fMLF-induced ERK1/2 phosphorylation. These results suggest that EGCG inhibits FPR-mediated leukocyte activation thus is a promising anti-inflammatory compound.lld:pubmed
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pubmed-article:19426837pubmed:authorpubmed-author:WangJi MingJMlld:pubmed
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pubmed-article:19426837pubmed:articleTitleThe green tea polyphenol (-)-epigallocatechin-3-gallate inhibits leukocyte activation by bacterial formylpeptide through the receptor FPR.lld:pubmed
pubmed-article:19426837pubmed:affiliationInstitute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, China.lld:pubmed
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pubmed-article:19426837pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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