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. 2022 Oct 26;15(3):765–795. doi: 10.1016/j.jcmgh.2022.10.014

Figure 1.

Figure 1

Loss of Nr1i2 (the gene encoding the pregnane X receptor) exacerbates colonic fibrosis and is accompanied by elevated GM-CSF levels and neutrophilic inflammation after injury. (A) WT(Nr1i2+/+) and Nr1i2-/- mice were administered DSS for 5 days to induce colonic injury and inflammation and then switched to regular drinking water and allowed to heal for an additional 25 days (∗indicates the different analysis time points). (B) Weight recovery and (C) gross colon length and thickness in WT(Nr1i2+/+) and Nr1i2-/- mice 25 days after withdrawal of DSS. (D) Representative images of Masson’s trichrome staining to indicate fibrosis in the colon of WT(Nr1i2+/+) and Nr1i2-/- mice (scale bar = 100 μm). (F) Heatmap of cytokines and chemokines detected in the serum 25 days after withdrawal of DSS (each tile represents an individual animal) and absolute levels of the most differentially produced cytokines in the serum between WT(Nr1i2+/+) and Nr1i2-/- mice (n = 4–5 per group). (G) Representative FACS plots of CD11b+Ly6G+ neutrophils and CD11b+Ly6CHi monocytes in the healing colonic lamina propria of WT(Nr1i2+/+) and Nr1i2-/- mice 10 days after withdrawal of DSS (n = 3 per water groups, n = 4 per DSS groups). Data are presented as mean ± standard error of the mean. Student t test (C, E, and F) and one-way analysis of variance with Tukey post hoc test (H). ∗P < .05, ∗∗P < .01, ∗∗∗P < .001.