In fact, DSS administration to IL-33 deficient mice results in less severe colitis than in WT controls, with decreased granulocyte infiltration (175), while exogenous administration of IL-33 to DSS-treated mice further aggravates colitis and induces the influx of neutrophils (176), suggesting a pathogenic role of IL-33, at least in an acute inflammatory setting. Here, IL33 is linked to colitis.