Figure 4.

Excessive large intestinal PA does not disturb the intestinal immune homeostasis in WT mice. (A) Long-term experimental setup: WT mice were left untreated (ctr) or repeatedly treated with V/M (2 times for 7 days at the age of 4 and 8 weeks) (V/M) before acute DSS colitis was induced at the age of 12 weeks (n = 6/group). (B) Overview on the V/M-mediated and DSS-mediated compositional dynamics in the intestinal microbiota of V/M-treated mice compared with ctr mice (family level). (C) Overview on the long-term impact of V/M treatment on the phylogenetic makeup (beta-diversity) of cecal microbiota and its response to DSS treatment. (D) Richness of the intestinal microbiota. (E) Relative abundance of Bacteroidaceae, Prevotellaceae, and Porphyromonadaceae in untreated versus V/M-treated WT mice before and after exposure to DSS. The number of mice in which the respective bacterial family was detected (prevalence) is depicted above the respective figure. Color code: purple = during V/M treatment, light red = post V/M treatment (after first and second V/M treatments), red = DSS treatment. (F) Kinetic of the fecal serine protease activity in untreated (ctr) versus V/M-treated (V/M) WT mice. (G) Body weight development in ctr and V/M-treated WT mice. (H) The left panel shows the development of the disease activity index after induction of acute colitis by DSS. The right panel shows representative hematoxylin-eosin stainings including the mean histopathological score of colonic tissue from DSS-treated ctr versus DSS-treated V/M-pretreated mice at Day 8 after the induction of DSS colitis. (I–K) Organ weight in DSS-treated ctr and V/M-pretreated WT mice. DAI, disease activity index.