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Epigallocatechin gallate reduces human monocyte mobility and adhesion in vitro
Author(s) -
Melgarejo Esther,
Medina Miguel Ángel,
SánchezJiménez Francisca,
Urdiales José Luis
Publication year - 2009
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2009.00452.x
Subject(s) - monocyte , ccr2 , integrin , microbiology and biotechnology , cell adhesion , chemistry , thp1 cell line , inflammation , adhesion , fibronectin , chemotaxis , population , immunology , receptor , pharmacology , biology , cell culture , chemokine , biochemistry , medicine , chemokine receptor , extracellular matrix , organic chemistry , environmental health , genetics
Background and purpose:  Monocytes/macrophages are an important population of immune inflammatory cells that have diverse effector functions in which their mobility and adhesion play a very relevant role. Epigallocatechin gallate (EGCG), a major component of green tea, has been reported to have anti‐allergic and anti‐inflammatory activities, but its effects on monocytes remain to be determined. Here we investigated the effects of EGCG on the migration and adhesion of monocytes. Experimental approach:  We used a human monocyte cell line (THP‐1) to analyse the effects of treatment with EGCG under non‐cytotoxic conditions on the expression levels of the monocyte chemotactic protein‐1 (MCP‐1) and of the MCP‐1 receptor (CCR2) and on the activation of β1 integrin. A functional validation was carried out by evaluating the inhibitory effect of EGCG on monocyte adhesiveness and migration in vitro . Key results:  Treatment of THP‐1 cells with EGCG decreased MCP‐1 and CCR2 gene expression, together with MCP‐1 secretion and CCR2 expression at the cell surface. EGCG also inhibited β1 integrin activation. The effects on these molecular targets were in agreement with the EGCG‐induced inhibition of THP‐1 migration in response to MCP‐1 and adhesion to fibronectin. Conclusions and implications:  Under our experimental conditions, EGCG treatment inhibited the migration and adhesion of monocytes. These inhibitory effects of EGCG on monocyte function should be considered as a promising new anti‐inflammatory response with a potential therapeutic role in the treatment of inflammation‐dependent diseases.

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