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. 2016 Oct 18;45(4):802-816.
doi: 10.1016/j.immuni.2016.09.008. Epub 2016 Sep 28.

Bile Acids Control Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome (VSports)

Chuansheng Guo  1 , Shujun Xie  2 , Zhexu Chi  1 , Jinhua Zhang  3 , Yangyang Liu  1 , Li Zhang  1 , Mingzhu Zheng  1 , Xue Zhang  4 , Dajing Xia  5 , Yuehai Ke  4 , Linrong Lu  1 , Di Wang  6
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Bile Acids Control Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome

VSports app下载 - Chuansheng Guo et al. Immunity. .
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Abstract

Reciprocal interactions between the metabolic system and immune cells play pivotal roles in diverse inflammatory diseases, but the underlying mechanisms remain elusive. The activation of bile acid-mediated signaling has been linked to improvement in metabolic syndromes and enhanced control of inflammation. Here, we demonstrated that bile acids inhibited NLRP3 inflammasome activation via the TGR5-cAMP-PKA axis. TGR5 bile acid receptor-induced PKA kinase activation led to the ubiquitination of NLRP3, which was associated with the PKA-induced phosphorylation of NLRP3 on a single residue, Ser 291. Furthermore, this PKA-induced phosphorylation of NLRP3 served as a critical brake on NLRP3 inflammasome activation. In addition, in vivo results indicated that bile acids and TGR5 activation blocked NLRP3 inflammasome-dependent inflammation, including lipopolysaccharide-induced systemic inflammation, alum-induced peritoneal inflammation, and type-2 diabetes-related inflammation. Altogether, our study unveils the PKA-induced phosphorylation and ubiquitination of NLRP3 and suggests TGR5 as a potential target for the treatment of NLRP3 inflammasome-related diseases VSports手机版. .

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