Erratum: Caspase-11 is expressed in the colonic mucosa and protects against dextran sodium sulfate-induced colitis

Abstract

Correction to: Mucosal Immunology (2014) 7, 1480–1491; doi: 10.1038/mi.2014.36 The seventh sentence of the Abstract should read: “DSS-induced tissue damage and inflammatory cell infiltration in the gut were markedly increased in caspase-11−/− mice, while release of the pyroptosis/necroptosis marker HMGB1 was abolished. Correction to: Mucosal Immunology (2014) 7, 1480–1491; doi: 10.1038/mi.2014.36 The seventh sentence of the Abstract should read: “DSS-induced tissue damage and inflammatory cell infiltration in the gut were markedly increased in caspase-11−/− mice, while release of the pyroptosis/necroptosis marker HMGB1 was abolished. Correction to:Mucosal Immunology (2014) 7, 1480–1491; doi: 10.1038/mi.2014.36 The seventh sentence of the Abstract should read: “DSS-induced tissue damage and inflammatory cell infiltration in the gut were markedly increased in caspase-11−/− mice, while release of the pyroptosis/necroptosis marker HMGB1 was abolished.” The authors regret the error. Caspase-11 is expressed in the colonic mucosa and protects against dextran sodium sulfate-induced colitisMucosal ImmunologyVol. 7Issue 6PreviewUlcerative colitis and Crohn's disease are major inflammatory syndromes that affect millions of patients. Caspase-11 confers protection against Gram-negative enteropathogens, but its role during colitis is unknown. Here, we show that caspase-11 was constitutively expressed in the colon, and that caspase-11-deficient (caspase-11−/−) mice were hypersusceptible to dextran sodium sulfate (DSS)-induced colitis. Notably, pro-inflammatory Prevotella species were strongly reduced in the gut microbiota of caspase-11−/− mice. Full-Text PDF Open Archive