Gut microbial metabolites as key mediators in inflammatory bowel disease

Figure 5 Effect of metabolites on gut permeability and inflammation in the colon of Muc2^-/- mice. A: Evaluation of metabolites toxicity by alanine aminotransferase and aspartate aminotransferase activity in blood; B: Effect of metabolites on intestinal permeability of Muc2^-/- mice, expressed in μg/mL of fluorescein isothiocyanate-dextran in blood; C: Effect of metabolites on n (%) of regulatory T cells in the mesenteric lymph nodes of Muc2^-/- mice; D: Effect of metabolites on expression of pro- and anti-inflammatory cytokines and Foxp3 transcriptional factor in colon of Muc2^-/- mice; E: Effect of metabolites on cytokine content in colon of Muc2^-/- mice; F: Effect of metabolites on expression of markers of pro-inflammatory M1 (CD80, iNOS) and anti-inflammatory M2 (CD209, Arginase-1) peritoneal macrophages. Values are shown as medians and interquartile range (from min to max). All assays were performed in one experiment, consisted of 4-11 biological replicates (mice) per group. ^aP < 0.05 vs the control (Muc2^-/- mice), ^bP < 0.01 vs the control (Muc2^-/- mice), ^cP < 0.05 vs Muc2^-/- mice treated with butyric, propionic, and valeric acids combination, Kruskal-Wallis test with post hoc Dunn’s test, corrected with Benjamini-Hochberg procedure. ALT: Alanine aminotransferase; AST: Aspartate aminotransferase; FITC: Fluorescein isothiocyanate; Treg: Regulatory T cells; But: Butyric acid; Prop: Propionic acid; Val: Valeric acid; BPV: Combination of butyric, propionic, and valeric acids; IL: Interleukin; TNF-α: Tumor necrosis factor-α.