title: Dietary supplementation with high dose of epigallocatechin-3-gallate promotes inflammatory response in mice.
abstract: Epigallocatechin-3-gallate (EGCG) from green tea has been indicated to have anti-inflammatory activity. However, most of the evidence is in vitro studies in which EGCG is often added at levels unachievable by oral intake. With few exceptions, in vivo studies along this line have been conducted in animal models of diseases, and the results are inconclusive. In this study, we fed C57BL/6 mice a diet containing 0%, 0.15%, 0.3% or 1% (w/w) EGCG for 6 weeks. Contrary to the assumption that EGCG would reduce inflammatory response, mice fed 0.15% and 0.3% EGCG diet exhibited no change while those fed 1% EGCG diet produced more proinflammatory cytokines tumor necrosis factor-α, interleukin (IL)-6, and IL-1β and lipid inflammatory mediator prostaglandin E(2) in their splenocytes and macrophages (MΦ) and less IL-4 in splenocytes. Spleens from the mice fed 1% EGCG diet also had higher proportions of regulatory T cells, MΦ, natural killer (NK) cells and NKT cells compared to those from mice fed the other diets. These results suggest that high intake of EGCG may induce a proinflammatory response, and this change may be associated with a disturbed homeostasis of immune cells involving changes in both function and number of specific immune cell populations. While the mechanisms and clinical significance for this effect of EGCG remain to be investigated further, these data suggest the need for defining accurate EGCG dose limits to induce an anti-inflammatory effect since current data indicate that higher doses would produce an inflammatory response.
authors.affiliation: Nutritional Immunology Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
authors.forename: Munkyong
authors.initials: M
authors.lastname: Pae
authors.forename: Zhihong
authors.initials: Z
authors.lastname: Ren
authors.forename: Mohsen
authors.initials: M
authors.lastname: Meydani
authors.forename: Fu
authors.initials: F
authors.lastname: Shang
authors.forename: Donald
authors.initials: D
authors.lastname: Smith
authors.forename: Simin Nikbin
authors.initials: SN
authors.lastname: Meydani
authors.forename: Dayong
authors.initials: D
authors.lastname: Wu
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D002392:Catechin / Q000008:administration & dosage / Q000031:analogs & derivatives*; D019587:Dietary Supplements; D015232:Dinoprostone / Q000032:analysis / Q000378:metabolism; D007249:Inflammation / Q000139:chemically induced* / Q000503:physiopathology; D053583:Interleukin-1beta / Q000032:analysis / Q000378:metabolism; D015850:Interleukin-6 / Q000032:analysis / Q000378:metabolism; D007694:Killer Cells, Natural / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D055611:Natural Killer T-Cells / Q000187:drug effects / Q000378:metabolism; D010936:Plant Extracts / Q000008:administration & dosage*; D013154:Spleen / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D013662:Tea / Q000737:chemistry; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism
chemical_list: D015415:Biomarkers; D053583:Interleukin-1beta; D015850:Interleukin-6; D010936:Plant Extracts; D013662:Tea; D014409:Tumor Necrosis Factor-alpha; D002392:Catechin; C045651:epigallocatechin gallate; D015232:Dinoprostone