Gut microbial metabolites as key mediators in inflammatory bowel disease

Figure 4 Muc2 knockout mice as an in vivo model of inflammatory bowel disease - increased intestinal permeability and colon inflammation. A and B: Differences in colon length between wild-type mice (C57BL/6) and mice with mucin 2 gene knockout (Muc2^–/–) mice; C: Hematoxylin-eosin (top panel) and alcian blue (bottom-panel)-stained colonic sections (10 × magnification) of C57BL/6 and Muc2^-/- mice; D: Intestinal permeability of C57BL/6 and Muc2^-/- mice, expressed in μg/mL of fluorescein isothiocyanate-dextran in blood; E: Expression of pro- and anti-inflammatory cytokines and Foxp3 transcriptional factor in colon of C57BL/6 and Muc2^-/- mice; F: Intestinal content of inflammatory interleukin-1β and anti-inflammatory interleukin-10 in C57BL/6 and Muc2^-/- mice; G: Regulatory T cells content in mesenteric lymph nodes in C57BL/6 and Muc2^-/- mice; H: Ratio of M1 (CD80, iNOS) and M2 (CD209, Arginase-1) peritoneal macrophages in C57BL/6 and Muc2^-/- mice. All assays were performed in two independent experiments, each consisting of 4-11 biological replicates (mice) per group. ^aP < 0.05, ^bP < 0.01 vs the control (C57BL/6 mice), Mann-Whitney U test. FITC: Fluorescein isothiocyanate; Treg: Regulatory T cells; IL: Interleukin; TNF-α: Tumor necrosis factor-α; TGF-β: Transforming growth factor β.