Location: Human Nutrition Research Center on Aging
Title: Dietary supplementation with high dose of epigallocatechin-3-gallate (EGCG) promotes inflammatory response in mice Authors
|Munkyong, Pae -|
|Zhihong, Ren -|
|Meydani, Mohsen -|
|Shang, Fu -|
|Smith, Donald -|
|Meydani, Simin -|
|Wu, Dayong -|
Submitted to: Journal of Nutritional Biochemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 7, 2011
Publication Date: May 14, 2012
Citation: Munkyong, P., Zhihong, R., Meydani, M., Shang, F., Smith, D., Meydani, S., Wu, D. 2012. Dietary supplementation with high dose of epigallocatechin-3-gallate (EGCG) promotes inflammatory response in mice. Journal of Nutritional Biochemistry. 23:526-531. Interpretive Summary: Research studies suggest that drinking green tea may suppress inflammation, which is considered an underlying cause of several chronic diseases. However, most of the research on green tea is based on cell studies and not on consumption of tea as part of the diet. Further, appropriate amounts of green tea needed to produce a health benefit are unknown. In this study, we fed mice a diet that contained varying percentages of an active component of green tea called Epigallocatechin-3-gallate (EGCG) for 6 weeks. We assumed that EGCG would reduce inflammation; in fact, those mice fed the highest dose of EGCG exhibited an inflammatory response. Given our findings, further research is needed to determine safe levels of tea for daily consumption since overconsumption of green tea products and possibly green tea, a popular beverage consumed world-wide for its health benefits, may have adverse effects on human health.
Technical 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 were fed a diet containing 0, 0.15, 0.3, or 1% (w/w) EGCG for 6 wk. 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 pro-inflammatory cytokines TNF-alpha, IL-6, and IL-1beta and lipid inflammatory mediator prostaglandin E2 in their splenocytes and macrophages (Mph) and less IL-4 in splenocytes. Spleens from the mice fed 1% EGCG diet also had higher proportions of regulatory T cells, Mph, 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 pro-inflammatory 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 remains to be investigated further, these data suggest the need for defining accurate EGCG dose limits to induce an anti-inflammatory effect since current data indicates that higher doses would produce an inflammatory response.