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

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.