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<p><i>Helicobacter</i> <i>pylori</i> (<i>H. pylori</i>) infection poses significant risks for gastric cancer and intestinal inflammation, yet effective prevention strategies for intestinal inflammation remain elusive. Here, we aimed to investigate the protective effects and underlying mechanisms of <i>Lactiplantibacillus plantarum</i> ZJ316 (<i>L. plantarum</i> ZJ316) in a mouse model of <i>H. pylori</i>-induced intestinal inflammation. The reverse transcription‑quantitative polymerase chain reaction (RT-qPCR) analysis showed that treatment with <i>L. plantarum</i> ZJ316 significantly upregulated the mRNA levels of tight junction proteins, including Zonula occludens-1 (ZO-1), Occludin, and Claudin-1, while simultaneously decreasing the expression levels of pro-inflammatory cytokines interleukin-1β (IL-1β), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α). Additionally, 16S rDNA sequencing analysis revealed that administration of <i>L. plantarum</i> ZJ316 reduced relative abundance of pathogenic bacteria, <i>Staphylococcus</i> and <i>Desulfovibrio</i> by 69% and 42%, respectively, while enhancing beneficial bacteria including <i>Ligilactobacillus</i>, <i>Akkermansia</i>, and <i>Lactobacillus</i> associated with short-chain fatty acids (SCFAs) synthesis by 88%, 85%, and 16%, respectively. Gas chromatography–mass spectrometry (GC–MS) analysis confirmed <i>L. plantarum</i> ZJ316 restored SCFA levels reduced by <i>H. pylori</i> infection. In vitro, <i>L. plantarum</i> ZJ316 inhibited the IκBα/NF-κB pathway, thereby reducing TNF-α and IL-8 production in HT-29 cells following <i>H. pylori</i> infection. These findings collectively suggest that <i>L. plantarum</i> ZJ316 ameliorates <i>H. pylori</i>-induced intestinal inflammation by enhancing gut barrier function, improving flora structure, increasing SCFA levels, and mitigating inflammation through NF-κB pathway inhibition, offering promise for therapeutic development.</p> Graphical Abstract <p><i>Helicobacter pylori</i>-induced intestinal inflammation in murine models is mitigated by intragastric administration of <i>Lactiplantibacillus plantarum </i>ZJ316. This strain antagonizes the NF-κB pathway; attenuates pro-inflammatory mediators such as IL-1β, TNF-α, and IFN-γ; and reinforces the intestinal mucosal barrier, exemplified by heightened levels of ZO-1, Occludin, Claudin, and MUC2. Furthermore, <i>L. plantarum</i> ZJ316 rectifies dysbiosis triggered by <i>H. pylori</i>, rebalancing the microbiota by diminishing pathogenic taxa, enriching commensal populations, and augmenting short-chain fatty acid production</p> <p></p>

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Lactiplantibacillus plantarum ZJ316 Alleviates Helicobacter pylori-Induced Intestinal Inflammation by Sustaining Intestinal Homeostasis

  • 期刊论文

  • 发表日期：

    2025年2月13日

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  • Shiying Wu,
  • Fangtong Wei,
  • Yongqiang Chen,
  • Ziqi Chen,
  • Yuenuo Luo,
  • Jiayi Fan,
  • Yang Xu,
  • Mingyang Hu,
  • Ping Li,
  • Qing Gu

摘要

Helicobacter pylori (H. pylori) infection poses significant risks for gastric cancer and intestinal inflammation, yet effective prevention strategies for intestinal inflammation remain elusive. Here, we aimed to investigate the protective effects and underlying mechanisms of Lactiplantibacillus plantarum ZJ316 (L. plantarum ZJ316) in a mouse model of H. pylori-induced intestinal inflammation. The reverse transcription‑quantitative polymerase chain reaction (RT-qPCR) analysis showed that treatment with L. plantarum ZJ316 significantly upregulated the mRNA levels of tight junction proteins, including Zonula occludens-1 (ZO-1), Occludin, and Claudin-1, while simultaneously decreasing the expression levels of pro-inflammatory cytokines interleukin-1β (IL-1β), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α). Additionally, 16S rDNA sequencing analysis revealed that administration of L. plantarum ZJ316 reduced relative abundance of pathogenic bacteria, Staphylococcus and Desulfovibrio by 69% and 42%, respectively, while enhancing beneficial bacteria including Ligilactobacillus, Akkermansia, and Lactobacillus associated with short-chain fatty acids (SCFAs) synthesis by 88%, 85%, and 16%, respectively. Gas chromatography–mass spectrometry (GC–MS) analysis confirmed L. plantarum ZJ316 restored SCFA levels reduced by H. pylori infection. In vitro, L. plantarum ZJ316 inhibited the IκBα/NF-κB pathway, thereby reducing TNF-α and IL-8 production in HT-29 cells following H. pylori infection. These findings collectively suggest that L. plantarum ZJ316 ameliorates H. pylori-induced intestinal inflammation by enhancing gut barrier function, improving flora structure, increasing SCFA levels, and mitigating inflammation through NF-κB pathway inhibition, offering promise for therapeutic development.

Graphical Abstract

Helicobacter pylori-induced intestinal inflammation in murine models is mitigated by intragastric administration of Lactiplantibacillus plantarum ZJ316. This strain antagonizes the NF-κB pathway; attenuates pro-inflammatory mediators such as IL-1β, TNF-α, and IFN-γ; and reinforces the intestinal mucosal barrier, exemplified by heightened levels of ZO-1, Occludin, Claudin, and MUC2. Furthermore, L. plantarum ZJ316 rectifies dysbiosis triggered by H. pylori, rebalancing the microbiota by diminishing pathogenic taxa, enriching commensal populations, and augmenting short-chain fatty acid production