IL18 and colitis: At odds with the above data, Demon et al. (53) suggested that sensitivity to DSS colitis in Casp11−/− mice is independent from caspase-1-induced canonical inflammasome activation, since the colonic levels of IL-1β and IL-18, as well as circulating HMGB1 in DSS Casp11−/− mice, did not differ from DSS WT mice, suggesting that caspase-11 protects against colitis independently from inflammasome activation and, therefore, hypothesizing an unidentified pathway for caspase-11 in bowel inflammation (Figure 2) (53).