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Anti-microbial signaling pathways are normally triggered by innate immune receptors when detecting pathogenic microbes to provide protective immunity. Here we show that the inflammasome sensor Nlrp1 aggravates DSS-induced experimental mouse colitis by limiting beneficial, butyrate-producing  Clostridiales  in the gut. The colitis-protective effects of  Nlrp1  deficiency are thus reversed by vancomycin treatment, but recapitulated with butyrate supplementation in wild-type mice. Moreover, an activating mutation in  Nlrp1a  increases IL-18 and IFNγ production, and decreases colonic butyrate to exacerbate colitis. We also show that, in patients with ulcerative colitis, increased  NLRP1  in inflamed regions of the colon is associated with increased  IFN-γ . In this context,  NLRP1 ,  IL-18  or  IFN-γ  expression negatively correlates with the abundance of  Clostridiales  in human rectal mucosal biopsies. Our data identify the NLRP1 inflammasome to be a key negative regulator of protective, butyrate-producing commensals, which therefore promotes inflammatory bowel disease.

NLRP1 restricts butyrate producing commensals to exacerbate inflammatory bowel disease