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The green tea polyphenol (-)-epigallocatechin-3-gallate inhibits leukocyte activation by bacterial formylpeptide through the receptor FPR

  1. Author:
    Zhu, J. J.
    Wang, O. M.
    Ruan, L. F.
    Hou, X. W.
    Cui, Y. H.
    Wang, J. M.
    Le, Y. Y.

  2. Author Address

    Zhu, Jingjing, Wang, Oumei, Ruan, Lingfei, Hou, Xinwei, Cui, Youhong, Le, Yingying] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Nutr & Metab, Shanghai 200031, Peoples R China. [Wang, Oumei, Ruan, Lingfei, Hou, Xinwei, Le, Yingying] Chinese Acad Sci, Grad Sch, Shanghai 200031, Peoples R China. [Wang, Ji Ming] NCI, Mol Immunoregulat Lab, Ctr Canc Res, Frederick, MD 21701 USA.
    1. Year: 2009
  2. Journal: International Immunopharmacology
    1. 9
    2. 9
    3. Pages: 1126-1130
  4. Type of Article: Article
  1. Abstract:

    Although 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. (C) 2009 Elsevier B.V. All rights reserved.

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  2. DOI: 10.1016/j.intimp.2009.05.002
  3. PMID: 19426837

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