期刊
BMC GASTROENTEROLOGY
卷 16, 期 -, 页码 -出版社
BIOMED CENTRAL LTD
DOI: 10.1186/s12876-016-0500-x
关键词
Butyrate; Inflammatory bowel disease; Cytokines; Th17; Treg
资金
- Beijing Renze Foundation [ZX IBD 13002]
- National Natural Science Foundation of China [81170359]
- Nanjing Foundation for Development of Science and Technology [YKK15232]
- Outstanding Youth Project of Nanjing City [JQX14005]
Background: Butyrate is an energy source for colonocytes that is formed by bacterial fermentation of dietary fiber in the colon and that exerts broad anti-inflammatory activities. Although the administration of butyrate improves homeostasis in patients and ameliorates IBD (Inflammatory Bowel Disease)-related lesions and symptoms, the anti-inflammatory mechanisms of butyrate still remain unclear. To explore the impact of butyrate on Treg (Regulatory T cell)/Th17 (T helper 17 cell) differentiation and colitis in rats. Methods: The effect of butyrate on the expression of markers related to both Tregs and Th17 cells were determined in human monocytes as well as a rat model of colitis induced by 2,4,6-trinitrobenzene sulfonic acid. Rats were treated with butyrate in vivo, whereas the rat splenocytes and human monocytes were treated in vitro. Results: We found that butyrate administration increased peripheral blood Treg cell levels as well as plasma levels of anti-Th17 cytokines (IL-10 and IL-12). Butyrate administration further suppressed IL-17 levels in both plasma and colonic mucosa, and ameliorated colonic colitis lesions in rats. This promotion of Treg activity and inhibition of IL-17 release was also observed in human venous monocytes and rat splenocytes in vitro. Conclusions: Our results suggest that butyrate plays a key role in regulating the Treg/Th17 balance and ultimately protects the colon mucosa against the development of IBD.
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