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<p>Enterotoxigenic <i>Escherichia coli</i> (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&#xa0;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., <i>Lactobacillus</i>), 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.</p> Graphical Abstract <p></p>

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

  • 期刊论文

  • 发表日期：

    2025年9月9日

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  • Chunjia Li,
  • Miao Wang,
  • Lixiao Duan,
  • Jinge Xin,
  • Xueqin Ni,
  • Dong Zeng,
  • Bangyuan Wu

摘要

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.

Graphical Abstract