Fig. 6: OSM signaling in epithelial cells promotes STAT3 activation.

a, Workflow schematic for scRNA-seq sample preparation (left) and volcano plot depicting differentially expressed genes in enterocytes between inflamed mice after colitis induction and steady-state (see Fig. 1d). Red dots represent genes that are expressed at least twofold higher with statistical significance. b, Significantly enriched (adjusted P < 0.05) gene set enrichment analysis (GSEA) terms in enterocytes from scRNA-seq data derived from a; adjusted P values were calculated using the Benjamini–Hochberg test. c, PROGENy pathway activity scores derived from epithelial scRNA-seq data. PROGENy is a computational method that leverages a large compendium of publicly available perturbation experiments to identify a core set of pathway responsive genes, enabling the inference of pathway activity from transcriptomic data. d, Left, experimental workflow of bulk RNA-seq of sorted epithelial cells from IEC^ΔOsmr and control mice. H. hepaticus + anti-IL-10R colitis was induced in IEC^ΔOsmr and control mice (littermates). IECs were sorted from both genotypes on day 21 and subjected to bulk RNA-seq. Right, volcano plot depicting differentially expressed genes in IECs between inflamed IEC^ΔOsmr and control mice (n = 5 per group). Red dots represent genes that are expressed at least twofold higher with statistical significance. e, Significantly enriched (adjusted P < 0.05) GSEA terms in epithelial cells from bulk RNA-seq data derived from d; adjusted P values were calculated using the Benjamini–Hochberg test. f, PROGENy pathway activity scores derived from epithelial bulk RNA-seq data in d.