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Bile acids control inflammation and metabolic disorder through inhibition of NLRP3 inflammasom

王迪  
【摘要】:Reciprocal interactions between the metabolic system and immune cells play pivotal roles in the pathogenesis of diverse inflammatory diseases,but the underlying mechanisms are still unclear.The activation of bile acid-mediated signaling has been linked to improvement in metabolic syndromes and enhanced control of inflammation.Here,we demonstrate that bile acids inhibit NLRP3 inflammasome activation via the TGR5-cAMP-PKA axis.TGR5 signaling induces PKA activation,which phosphorylates NLRP3 on a single residue,Ser 291.Importantly,the PKA-induced phosphorylation of NLRP3 on Ser 291 leads to the ubiquitination of NLRP3,and this serves as a critical brake on NLRP3 inflammasome activation.In addition,in vivo results indicate that bile acids and TGR5 activation block 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 subsequent ubiquitination of NLRP3 and suggests TGR5 as a potential target for the treatment of NLRP3 inflammasome-related diseases.

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