DSS administration to IL-33-deficient mice resulted in less severe colitis than in wild-type (WT) controls, with decreased granulocyte infiltration[42], while exogenous administration of IL-33 to DSS-treated mice further aggravated colitis and induced influx of neutrophils[44], suggesting a pathogenic role of IL-33, at least in an acute inflammatory setting. This evidence concerns the gene IL33 and colitis.