Fig. 2.

Stat6 deletion increases DSS-induced colitis severity a–n. a–m The mice were subjected to one i.p. injection of AOM (day 0) and exposed to 2% DSS in the drink water for five days (days 5–10), being killed after 5 days of recovery in normal water (day 15). a Representative H&E stained sections of colons from WT and Stat6^−/− mice (H&E); b, c Histological scoring of mucosal damage, inflammation and ulceration in WT and Stat6^−/− mice at day 15 of the AOM/DSS model (WT n = 5; Stat6^−/− n = 9); d–f RT-PCR, expression analysis of inflammation-related and M2/M1 genes in the mucosa of unchallenged (day 0) and AOM/DSS-treated mice at day 15 (WT d0/Stat6^−/− d0 n = 3; WT d15/Stat6^−/− d15 n = 5); g, h Immunohistochemical analysis and quantification of p-STAT3 Y705 performed with colonic sections of WT and Stat6^−/− mice (WT d15 n = 5; Stat6^−/− d15 n = 4); i, j Immunohistochemical analysis and quantification for BrdU incorporation in WT and Stat6^−/− mice (WT d15 n = 5; Stat6^−/− d15 n = 9); k Representative H&E stained sections from colons of Stat6^−/− and Stat3^ΔIEC; Stat6^−/− double knockout mice at day 15 of AOM/DSS model; l Quantification of areas of total crypt loss in Stat6^−/− and Stat3^ΔIEC; Stat6^−/− double knockout at day 15 of AOM/DSS model (Stat6^−/− d15 n = 16; Stat3^ΔIEC; Stat6^−/− d15 n = 15); m Index of p-Histone H3 expressing IEC in Stat6^−/− and Stat3^ΔIEC; Stat6^−/− double knockout mice at day 15 of the AOM/DSS model (Stat6^−/− d15 n = 5; Stat3^ΔIEC; Stat6^−/− d15 n = 10); n Tumor incidence in Stat6^−/− (n = 7) and Stat3^ΔIEC; Stat6^−/− mice (n = 10) at the end of the CAC model. Animals were exposed to reduced DSS concentration during the CAC cycles to prevent mortality (0.5%, 0.8 and 1% DSS, respectively). Data are mean ± SEM