Fig. 2

Development of intestinal inflammation requires both the pathobiont, H. bilis, as well as commensal bacteria in the context of host immune dysregulation. A, B WT and Was^−/− mice were colonized with the indicated gut microbial communities. A Representative H&E-stained formalin-fixed paraffin-embedded proximal colon sections at 20 weeks after colonization. 20× magnification, scale bars = 100μm. B Quantitative histological colitis scores at 20 weeks after colonization (n = 5,4,5,5,6,3,8,8). C–E Germ-free WT/HET (n=28) and Was^−/− (n = 21) mice were colonized with the ASF community and a subset (WT/HET (n = 17) and Was^−/− (n = 13)) were gavaged with H. bilis. C Spleen weights were measured 20 weeks after gavage with H. bilis. Colonic lamina propria lymphocytes were isolated 20 weeks after infection with H. bilis, and percentages of IL17-A⁺ CD4 T cells (D) and IL-22⁺ ILC3s (E) were determined by flow cytometry. Statistics performed using Student’s t-test. *p < 0.05, ***p < 0.001