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. 2015 Dec;185(12):3290–3303. doi: 10.1016/j.ajpath.2015.08.015

Figure 1.

Figure 1

Cecal and colonic pathology after type 17 helper T-cell cytokine blockade in Helicobacter hepaticus (Hh)–induced intestinal inflammation. C57BL/6 wild-type (WT) mice were inoculated with H. hepaticus and treated with anti–IL-10 receptor (IL-10R) monoclonal antibody (mAb) plus neutralizing mAb to IL-17A, IL-17F, IL-17A + IL-17F, IL-22, or isotype control (Contr) on days 0, 7, and (if applicable) 14 postinfection (pi). One week after the last mAb administration, pathology was analyzed in the cecum and ascending colon. A and B: Histology scores of cecum (A) and ascending colon (B) using a scoring system on the basis of 20 parameters of inflammation, as described in Materials and Methods. Each symbol represents an individual mouse. Data are pooled from two separate experiments analyzed at 2 and 3 weeks pi, respectively. C–N: Histology of representative cecal (C–H) and colonic (I–N) sections from the mice in A and B. Uninfected (Uninf.) WT (C and I), H. hepaticus–infected WT plus anti–IL-10R plus control mAb (D and J), H. hepaticus–infected WT plus anti–IL-10R plus anti–IL-17A (E and K), H. hepaticus–infected WT plus anti–IL-10R plus anti–IL-17F (F and L), H. hepaticus–infected WT plus anti–IL-10R plus anti–IL-17A plus anti–IL-17F (G and M), and H. hepaticus–infected WT plus anti–IL-10R plus anti–IL-22 (H and N). Hematoxylin and eosin staining was used. O and P: Histology scores of cecum (O) and ascending colon (P) using a scoring system on the basis of five parameters of inflammation [epithelial hyperplasia, lamina propria (LP) cellularity, goblet cell depletion, crypt abscesses, and ulcers]. Each symbol represents an individual mouse. Data are pooled from two separate experiments analyzed at 2 weeks pi. ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001. Scale bar = 100 μm (C–N).