Lactobacillus plantarum with lignin prevents Helicobacter pylori mediated DSS-colitis through improved intestinal integrity and reducing colonic inflammation in C57BL/6J mice.

Abstract

Background: Probiotics are beneficial microorganisms that affect stomach acid and reduce bile production in the host organism. Helicobacter pylori infection causes chronic gastritis, peptic ulcer, gastric carcinoma and gastric lymphoma. Probiotic mediated gut health improvement in H. pylori infection remains underestimated.

Objective: The study aimed to develop Venu Lactiplantibacillus plantarum (VLP) surface coated with lignin and examine their protective effects and metabolic pathways in a colitis model using dextran sulphate sodium (DSS) in male C57BL/6J mice.

Materials and methods: The toxic effects of dietary lignin were assessed on H. pylori and L. plantarum (VLP) using bacterial growth optical density (OD) at 600 nm. C57BL/6J male mice were induced with DSS colitis with H. pylori antigens and VLP with lignin was used to reduce the gut colitis by examined the length of the colon, the presence of inflammation, and the level of oxidative stress in mice. The collapse of the intestinal barrier was further identified by investigating gut permeability and inflammatory markers such as tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interferon-γ (IFN-γ), and transforming growth factor-β (TGF-β) using enzyme linked immunosorbent assay (ELISA) platform methods.

Result: The toxic effects of dietary lignin were assessed and it was found that lignin treatment exhibited substantial inhibition against H. pylori inhibition at a dose of 5 μmol/L and the OD value at 600 nm. The viability of VLPs treated with lignin exhibited a 2.0 CFU/mL with significant increase in viable growth after a period of 3 h. The findings demonstrated that the application of L. plantarum with lignin treatment effectively decreased the levels of inflammatory cytokines in colon tissues affected by inflammation. The ulcerative colitis disease activity index was greatly lowered by modulating the immunological response, boosting antioxidant capacity, and regulating inflammatory signalling pathways. In vitro experiments demonstrated that VLP-treated Caco-2 cells effectively decreased H. pylori infection and enhanced their survival ability, invasion, and adhesion.

Conclusion: To summarize, the presence of lignin in VLP has the ability to alleviate colitis generated by DSS and H. pylori antigens, and its therapeutic capabilities against ulcerative colitis in a mouse model have been investigated. © 2025 Society of Chemical Industry.