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<p>Probiotics show potential for preventing and mitigating inflammatory bowel disease (IBD), though their efficacy and mechanisms are strain-specific. This study aimed to elucidate the protective mechanism of <i>Lactiplantibacillus</i> (<i>L.</i>) <i>plantarum</i> P16 against dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). The strain exhibited high gastrointestinal tolerance, with survival rates of approximately 86% in artificial gastric fluid (pH 3.0) and 94% in 0.3% bile salt after 3&#xa0;h of incubation. Moreover, <i>L. plantarum</i> P16 showed stronger adhesion to Caco-2 cells, indicating a high potential for intestinal colonization. In a DSS-induced colitis model, <i>L. plantarum</i> P16 administration alleviated colitis by reducing the disease activity index (DAI), suppressing pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), and mitigating colonic tissue damage while preserving epithelial barrier integrity. Additionally, <i>L. plantarum</i> P16 treatment increased short-chain fatty acid (SCFA) levels. 16&#xa0;S rRNA amplicon sequencing of cecal content revealed that <i>L. plantarum</i> P16 supplementation restored gut microbial homeostasis by elevating the abundances of <i>Firmicutes</i> and <i>Verrucomicrobiota</i>, particularly <i>Akkermansia</i>, while reducing the proportions of <i>Bacteroides</i> and <i>Helicobacter</i>. These findings demonstrated that <i>L. plantarum</i> P16 could alleviate colitis by ameliorating intestinal inflammation and restoring gut microbiota dysbiosis, proposing a novel perspective of <i>L. plantarum</i> P16 for UC management.</p>

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Lactiplantibacillus plantarum P16 mitigated murine colitis through modulation of immune response and gut microbiota

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月17日

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  • Zhixian Chen,
  • Qian Cheng,
  • Xiaoli Zhang,
  • Zhouhuang Sheng,
  • Lei Shi,
  • Yan Zhang

摘要

Probiotics show potential for preventing and mitigating inflammatory bowel disease (IBD), though their efficacy and mechanisms are strain-specific. This study aimed to elucidate the protective mechanism of Lactiplantibacillus (L.) plantarum P16 against dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). The strain exhibited high gastrointestinal tolerance, with survival rates of approximately 86% in artificial gastric fluid (pH 3.0) and 94% in 0.3% bile salt after 3 h of incubation. Moreover, L. plantarum P16 showed stronger adhesion to Caco-2 cells, indicating a high potential for intestinal colonization. In a DSS-induced colitis model, L. plantarum P16 administration alleviated colitis by reducing the disease activity index (DAI), suppressing pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), and mitigating colonic tissue damage while preserving epithelial barrier integrity. Additionally, L. plantarum P16 treatment increased short-chain fatty acid (SCFA) levels. 16 S rRNA amplicon sequencing of cecal content revealed that L. plantarum P16 supplementation restored gut microbial homeostasis by elevating the abundances of Firmicutes and Verrucomicrobiota, particularly Akkermansia, while reducing the proportions of Bacteroides and Helicobacter. These findings demonstrated that L. plantarum P16 could alleviate colitis by ameliorating intestinal inflammation and restoring gut microbiota dysbiosis, proposing a novel perspective of L. plantarum P16 for UC management.