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BMC Gastroenterol. 2016 Jul 30;16(1):84. doi: 10.1186/s12876-016-0500-x.

Butyrate inhibits interleukin-17 and generates Tregs to ameliorate colorectal colitis in rats.

Author information

1
Department of Gastroenterology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, China.
2
Department of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, China.
3
School of Life Sciences, Fudan University, Shanghai, China.
4
Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
5
Department of Gastroenterology, Nanjing Jiangbei People's Hospital Affiliated to Southeast University Medical School, Nanjing, China.
6
Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
7
State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.
8
Department of Digestive Diseases, Huashan Hospital, Fudan University, Shanghai, China. archsteed@163.com.
9
Department of Gastroenterology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, China. chenggong-yu@nju.edu.cn.

Abstract

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.

KEYWORDS:

Butyrate; Cytokines; Inflammatory bowel disease; Th17; Treg

PMID:
27473867
PMCID:
PMC4967301
DOI:
10.1186/s12876-016-0500-x
[Indexed for MEDLINE]
Free PMC Article

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