Effects and Mechanisms of Lactiplantibacillus plantarum G83 on Enterotoxigenic Escherichia coli (ETEC)-Induced Intestinal Inflammation.

Enterotoxigenic Escherichia coli (ETEC) is a prevalent intestinal pathogen that significantly impacts both human and animal health. G83, isolated from giant panda feces, has demonstrated notable probiotic properties. In this study, C57BL/6 J mice were randomly divided into Control, ETEC, and G83 groups. Experimental included monitoring body weight, assessing fecal occult blood, histopathological examination of ileal tissues, and quantification of antioxidant markers (SOD, T-AOC, MDA) in ileal tissues. Furthermore, real-time quantitative PCR was utilized to determine mRNA expression levels of inflammatory cytokines (TNF-α, IL-17, IL-10), tight junction proteins (Claudin, ZO-1, Occludin), mucin (Muc2), and lysozyme (Lyz-1). Transcriptomic bioinformatics analysis and 16S rRNA sequencing were integrated to characterize host gene expression profiles and gut microbial compositional dynamics, respectively. The results revealed that G83 alleviated ETEC-induced weight loss, reduced fecal occult blood, and mitigated ileal structural injuries. Additionally, G83 significantly enhanced intestinal antioxidant capacity by increasing T-AOC and SOD levels. Mechanistically, G83 downregulated pro-inflammatory cytokines TNF-α and IL-17 and the levels of Muc2 and Lyz1, while upregulating the expression of tight junction proteins ZO-1, Claudin, and Occludin. Transcriptomic analysis suggests that ETEC triggers inflammasome activation and initiates inflammatory responses by significantly upregulating Aim2. Conversely, G83 exerts protective effects by modulating the immune regulatory network-specifically, by significantly downregulating C3 expression to activate the complement system and participating in mucosal immune remodeling. Enrichment analysis reveals that G83 alleviates ETEC-induced intestinal inflammation primarily by inhibiting the NF-κB pathway and enhancing the intestinal IgA immune network. Additionally, 16S rRNA analysis indicates that G83 may improve ETEC-induced alterations in microbial community structure by increasing the abundance of beneficial bacteria (e.g., Lactobacillus), thereby further ameliorating impairment of intestinal microbial barrier function in mice. These findings provide a scientific basis for using G83 to ameliorate ETEC-mediated intestinal inflammation.