Fig. 2: DRD5 deficiency in immune cells exacerbates DSS-induced colitis.
From: DA-DRD5 signaling controls colitis by regulating colonic M1/M2 macrophage polarization

A, B Age-matched male WT and DRD5−/− mice (n = 9 mice per group) were given 2.5% DSS in their drinking water for 6 days and distilled water for three additional days before sacrifice. Weight changes (A) and disease activity index (DAI) (B) were monitored daily. C Gross morphology images of colons and colon lengths of WT and DRD5−/− mice on day 9 after DSS treatment. D Representative H&E-stained colonic sections and histology scores of WT and DRD5−/− mice sampled on day 9 after DSS treatment. Scale bars, 4×, 500 μm; 20×, 200 μm. E The concentration of TNF-α, IL-6, and CCL2 in the serum of WT and DRD5−/− mice were measured by ELISA. F, G Weight changes (F) and disease activity index (DAI) (G) after DSS-induced colitis in WT and DRD5−/− mice (n = 5 mice per group) adoptively transferred with WT or DRD5−/− bone marrow cells. H Gross morphology images of colons and colon lengths of WT and DRD5−/− mice adoptively transferred with WT or DRD5−/− bone marrow cells on day 9 after DSS treatment. I Representative H&E staining of colonic sections and histology scores of WT and DRD5−/− mice adoptively transferred with WT or DRD5−/− bone marrow cells on day 9 after DSS treatment. Scale bars, 4×, 500 μm; 20×, 200 μm. J The concentration of TNF-α, IL-6, and CCL2 in the serum of WT and DRD5−/− mice (n = 5 mice per group) adoptively transferred with WT or DRD5−/− bone marrow cells after DSS treatment. Data are pooled from three independent experiments. Error bars show means ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001. multiple unpaired t-tests for (A, B, F, G) and two-tailed unpaired student’s t-test for (C–E). One-way ANOVA with Sidak’s multiple comparisons test for (H–J).