Promotes Recovery of the Colon Barrier in Septic Mice through Accelerating ISCs Regeneration.

Disruption of the intestinal barrier is both the cause and result of sepsis. The proliferation and differentiation of intestinal stem cells (ISCs) promote the regenerative nature of intestinal epithelial cells, repairing the injured intestinal mucosal barrier; however, it is uncertain whether the recovery effects mediated by the ISCs are related to the gut microbiota. This research found that the survival rate of septic mice was improved with a () treatment. Furthermore, an increased proliferation and decreased apoptosis in colon epithelial cells were observed in the -treated septic mice. In vitro, we found that a supernatant was effective in maintaining the colonoid morphology and proliferation under the damage of TNF-α. Both in the mice colon and the colonoid, the -induced barrier repair process was accompanied by an increased expression of Lgr5 and lysozyme cells. This may be attributed to the upregulation of the IL-17, retinol metabolism, NF-kappa B and the MAPK signaling pathways, among which, Tnfaip3 and Nfkbia could be used as two potential biomarkers for in intestinal inflammation therapy. In conclusion, our finding suggests that protects a sepsis-injured intestinal barrier by promoting ISCs regeneration, highlighting the protective mechanism of oral probiotic consumption in sepsis.