Figure 1. NLR inflammasome components attenuate acute ulcerative colitis. (A) Schematic of the acute model of DSS-induced ulcerative colitis. (B) Kaplan-Meier plot of WT, Nlrp3−/−, Pycard−/−, and Casp1−/− mouse survival. (C) Weight loss of WT, Nlrp3−/−, and Pycard−/− mice. (D) Clinical parameters (weight loss, stool consistency, bleeding) of indicated mice. Data shown are representative of at least three independent experiments and depict the mean ± SEM. The symbols # and § indicate P < 0.05 and P < 0.01, respectively, between the mock- and DSS-treated WT; * indicates P < 0.05 between the DSS-treated gene-deficient strains compared with DSS-treated WT. WT mock, n = 4; DSS-treated WT, n = 14; Pycard−/−, n = 4; Nlrp3−/−, n = 6; Casp1−/−, n = 4. Casp1−/− animals were highly sensitive to the acute administration of DSS and were not subjected to additional monitoring described in C and D for humane reasons.
Figure 1.

NLR inflammasome components attenuate acute ulcerative colitis. (A) Schematic of the acute model of DSS-induced ulcerative colitis. (B) Kaplan-Meier plot of WT, Nlrp3−/−, Pycard−/−, and Casp1−/− mouse survival. (C) Weight loss of WT, Nlrp3−/−, and Pycard−/− mice. (D) Clinical parameters (weight loss, stool consistency, bleeding) of indicated mice. Data shown are representative of at least three independent experiments and depict the mean ± SEM. The symbols # and § indicate P < 0.05 and P < 0.01, respectively, between the mock- and DSS-treated WT; * indicates P < 0.05 between the DSS-treated gene-deficient strains compared with DSS-treated WT. WT mock, n = 4; DSS-treated WT, n = 14; Pycard−/−, n = 4; Nlrp3−/−, n = 6; Casp1−/−, n = 4. Casp1−/− animals were highly sensitive to the acute administration of DSS and were not subjected to additional monitoring described in C and D for humane reasons.

This Feature Is Available To Subscribers Only

or Create an Account

Close Modal
Close Modal