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Effects of epigallocatechin gallate on regulatory T cell number and function in obese versus lean volunteers
Author(s) -
Yun JungMi,
Jialal Ishwarlal
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.541.11
Subject(s) - foxp3 , inflammation , flow cytometry , regulatory t cell , epigallocatechin gallate , immunology , in vivo , endocrinology , medicine , cancer research , pharmacology , t cell , chemistry , biology , immune system , il 2 receptor , biochemistry , microbiology and biotechnology , polyphenol , antioxidant
Obesity is associated with increased inflammation. Regulatory T cells (Tregs) are essential negative regulators of inflammation. Animal models of obesity are associated with decreased Tregs. Dietary modulation of Tregs could be used as a therapeutic strategy to control inflammation. Epigallocatechin gallate (EGCG) is a potent anti‐inflammatory agent and is suggested to have a role as a preventive agent in obesity, diabetes, and cardiovascular disease. The role of EGCG in modulation of Tregs has however not been studied. Thus, the aim of this study was to determine the effect of EGCG on Tregs number and function in obese and lean human subjects in vitro, and to delineate its specific regulation mechanisms. Tregs were isolated from normal and obese subjects and cultured in the absence or presence of EGCG (20 μM) for 24 h. Foxp3 +Tregs were enumerated using flow cytometry. Histone deacetylases (HDACs) expression and NF‐κBp65 activity were measured by ELISA and western blots. Obese subjects had lower Tregs and IL‐10 production than lean subjects. EGCG significantly enhanced Foxp3 expressing‐Tregs number and IL‐10 production ex vivo (p<0.05). Also, EGCG decreased NF‐κB activity and increased HDACs activity and HDAC 2 expression in Tregs (p<0.05) in both groups. Thus, EGCG enhances Tregs function and number by suppressing NF‐κB signaling pathway via epigenetic changes.