Fig. 4

Hyper-activation of Nlrp1 exacerbates DSS-induced colitis independent of IL-1R signaling. Il-1r^−/−Nlrp1a^Q593P/+ and Il-1r^−/−Nlrp1a^Q593P/Q593P mice were given 3% (w/v) DSS for 6 days. a The percentage weight loss, b colon length and c histology score for epithelial damage and inflammatory cell infiltrate of H&E-stained sections of the colon were measured for disease severity. d Representative H&E-stained sections of the distal colon from Il-1r^−/−Nlrp1a^Q593P/+ and Il-1r^−/−Nlrp1a^Q593P/Q593P mice, scale bar = 2 mm. Short chain fatty acid analysis was performed on fecal samples collected from WT and Nlrp1^−/− mice before (UT) and after vancomycin treatment. The concentrations of e butyrate and f propionate were measured by gas chromatography mass spectrometry. Data are representative of 2 independent experiments with 3–5 mice per group. Means ± SEM; *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001. As determined by a two-tailed, unpaired t-test