Alterations in Gut Microbiota and their Association with Colonic Permeability and Inflammation in LPS-induced Sepsis Mice.

Sepsis is a leading cause of death in critically ill patients. This study aimed to investigate alterations in the gut microbiota and their mechanisms of action in a mouse model of sepsis. 20 mice were exposed to saline, while 70 mice were exposed to lipopolysaccharides (LPS). The diversity, structure, and composition of the gut microbiota were examined using 16S rRNA sequencing on days 1, 3, 5, and 7. Immunohistochemistry was used to measure the expressions of the tight junction proteins zonula occludens-1 (ZO-1) and occludin to assess intestinal barrier damage. An enzyme-linked immunosorbent assay (ELISA) was used to measure the serum levels of interleukin-17 (IL-17) and interleukin-23 (IL-23) to assess the degree of inflammation. Over time, mice exposed to LPS exhibited marked dysbiosis of the intestinal microbiota, characterized by changes in microbiota composition. This was primarily due to the colonization of pathogenic bacteria belonging to the phylum Proteobacteria, and a significant decrease in the relative abundances of beneficial bacteria belonging to the phyla Firmicutes and Bacteroidetes. Additionally, the structure of the intestinal microbiota in LPS-treated mice was altered, resulting in a significant reduction in diversity. Bacteroides was identified as a biomarker through genus-level LEfSe analysis. The expressions of colonic occludin and ZO-1 were significantly downregulated, while the level of IL-17 was elevated in LPS-treated mice. The results of this study suggest that the gut microbiota undergoes changes during a week of sepsis in mice and that microbiota dysfunction may be closely related to intestinal barrier dysfunction and changes in the IL-17/IL-23 axis.