Figure 7.
GPR183 Expressed on Innate Immune Cells Promotes Colitis
(A) Colonic Ch25h, Cyp7b1, and Hsd3b7 mRNA expression in Rag1−/− mice injected with 100 μg CD40 Ab (n = 6–7). d, day.
(B) Transwell migration of GPR183-transduced B cell line (M12-GPR183-GFP) to colon homogenates from CD40-Ab-treated Rag1−/− mice (n = 4). Chemotaxis of GFP− M12 cells was used as a negative control.
(C) Correlation of CH25H, CYP7B1, and HSD3B7 with CXCL8 mRNA expression in the colon of healthy controls (black dots; n = 8) and patients with ulcerative colitis (red dots; n = 6).
(D) Immunofluorescence microscopy of proximal colon from Rag1-deficient Gpr183GFP/+ mice 7 days after CD40 Ab injection. Sections were co-stained for detection of nuclei (DAPI) and myeloid cells (CD11c) or ILCs (CD90.2). Inflammatory foci are shown. Scale bars (red) represent 100 μm.
(E) H&E staining of proximal colon from Rag1-deficient Gpr183+/+ and Gpr183−/− mice 7 days after CD40 Ab treatment. Inflammatory foci at the tip of colonic folds are indicated. Scale bars (blue) represent 500 μm.
(F) Number of inflammatory foci and colitis score in CD40-Ab-treated Gpr183+/+Rag1−/− and Gpr183−/−Rag1−/− mice (n = 7–15). PBS-treated Gpr183+/+Rag1−/− mice were used as controls.
Data are represented as means ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 by one-way ANOVA with Tukey’s post-test. Data are representative of or combined from two experiments.