Figure 2.

Signalling through IL-20RA and IL-20RB controls experimental DSS-induced colitis. (A) Normal appearance of colon cross-sections of WT, Il20ra^−/− and Il20rb^−/− mice in steady state (water without (w/o) DSS). (B) Experimental colitis (three independent experiments) was induced by the administration of 2% DSS in the drinking water for 7 days in WT (n=16), Il20ra^−/− mice (n=15) and Il20rb^−/− mice (n=14). Body weight loss during colitis course respective to day 0 (set as 100%). High-resolution mini-endoscopy pictures indicating the degree of intestinal inflammation and histological analysis of inflammation based on H&E staining. Scores were calculated as described in the online supplemental file. Shortened colon lengths indicate aggravation of inflammation. (C) Representative colon cross-sections of mice with DSS-induced colitis that have been stained with the pan-leucocyte marker CD45, the F4/80 macrophage marker and the goblet cell marker Ulex are presented in confocal images. (D–E) RNA-Seq analysis of Il20ra^−/− (n=3) and Il20rb^−/− (n=3) samples respective to WT control mice (n=5). (D) Expression levels for transcripts that are co-upregulated and co-downregulated in both KO mouse strains versus WT controls from one DSS experiment. (E) Most genes that were found to be co-upregulated in the KO strains could be grouped to Gene Ontology processes that are classically involved in the progression of DSS-induced colitis (left side panel) whereas the most co-downregulated genes did not readily point out to known Gene Ontology categories and are presented in alphabetical order in the panel on the right side. Scale bars, 100 µm in A and C, 50 µm in B. Statistics: analysis of variance corrected for multiple comparisons in B, mean with SEM or 95% CI is displayed; squared Pearson’s correlation coefficient (r) of the linear regression analysis in D. DSS, dextran sulfate sodium; IL, interleukin; KO, knockout; RNA-Seq, RNA-sequencing; WT, wildtype. *P<0.05; **p<0.01; ***p<0.001; ****p<0.0001.