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

Abstract

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.