丁酸盐
炎症
烟酸
生物
结直肠癌
肠道菌群
受体
癌症研究
结肠炎
免疫学
癌症
内分泌学
生物化学
发酵
遗传学
作者
Nagendra Singh,Ashish Gurav,Sathish Sivaprakasam,Evan K. Brady,Ravi N. Padia,Huidong Shi,Muthusamy Thangaraju,Puttur D. Prasad,Santhakumar Manicassamy,David H. Munn,Jeffrey R. Lee,Stefan Offermanns,Vadivel Ganapathy
出处
期刊:Immunity
[Elsevier]
日期:2014-01-01
卷期号:40 (1): 128-139
被引量:1773
标识
DOI:10.1016/j.immuni.2013.12.007
摘要
Summary
Commensal gut microflora and dietary fiber protect against colonic inflammation and colon cancer through unknown targets. Butyrate, a bacterial product from fermentation of dietary fiber in the colon, has been implicated in this process. GPR109A (encoded by Niacr1) is a receptor for butyrate in the colon. GPR109A is also a receptor for niacin, which is also produced by gut microbiota and suppresses intestinal inflammation. Here we showed that Gpr109a signaling promoted anti-inflammatory properties in colonic macrophages and dendritic cells and enabled them to induce differentiation of Treg cells and IL-10-producing T cells. Moreover, Gpr109a was essential for butyrate-mediated induction of IL-18 in colonic epithelium. Consequently, Niacr1−/− mice were susceptible to development of colonic inflammation and colon cancer. Niacin, a pharmacological Gpr109a agonist, suppressed colitis and colon cancer in a Gpr109a-dependent manner. Thus, Gpr10a has an essential role in mediating the beneficial effects of gut microbiota and dietary fiber in colon.
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