Fig. 2: OSMR expression in epithelial cells promotes intestinal inflammation.
From: The IL-22–oncostatin M axis promotes intestinal inflammation and tumorigenesis
a, Schematic illustrating the Osmr deletion strategy in different cell types. Cell-type-specific deleter mouse lines (VilcreERT2, Cdh5cre and Col1a2creERT2) were crossed with Osmrfl/fl mice to generate the indicated cell-type-specific Osmr knockouts. b, Timeline of tamoxifen administration and subsequent colitis induction. Respective littermate control mice (VilcreERT2–, Cdh5cre– or Col1a2creERT2– crossed with Osmrfl/fl or VilcreERT+, Cdh5cre+ or Col1a2creERT2+ crossed with Osmrfl/wt) were used for each genotype. c, Histopathological scoring 21 days after colitis induction, based on two to three independent experiments (control inflamed, n = 31; IECΔOsmr, n = 13; StromaΔOsmr, n = 21; EndoΔOsmr, n = 12). Adjusted P values calculated from a Kruskal–Wallis test with Dunn’s post hoc comparisons indicate differences between OSMR-deficient and wild-type mice. d, Representative hematoxylin and eosin-stained colon sections from steady-state and inflamed mice of the indicated genotypes at day 21; scale bar, 100 μm. Sample sizes are as indicated in c. e,f, Calprotectin (e) and lipocalin (f) levels in fecal samples from the indicated genotypes, measured by enzyme-linked immunosorbent assay (ELISA) and normalized to their respective inflamed control mice. Data were pooled from two independent experiments (IECΔOsmr, n = 12; StromaΔOsmr, n = 12; EndoΔOsmr, n = 14). P values (two-tailed) were calculated by one-sample t-tests and Wilcoxon tests. g, Differentially expressed genes in colonic tissues (RNA-seq) of the indicated mouse lines compared to either steady-state mice or respective inflamed controls; WT, wild-type. h, Heat map displaying the expression of curated IBD pathway genes in colon tissue of the different mouse genotypes (n = 4–5 per group). i, Top biological processes enriched among differentially expressed genes in colon tissue from IECΔOsmr mice compared to respective inflamed controls (n = 4–5 per group); Padj, adjusted P value.
