Ameliorates Dextran Sulfate Sodium-Induced Colitis by Producing Conjugated Linoleic Acid, Protecting Intestinal Mechanical Barrier, Restoring Unbalanced Gut Microbiota, and Regulating the Toll-Like Receptor-4/Nuclear Factor-κB Signaling Pathway.

This study aimed to explore the effects and differences of conjugated linoleic acid (CLA)-producing on the alleviation of dextran sulfate sodium (DSS)-induced colitis and to explore its patterns. Different strains were administered at 10 cfu/day 7 days before DSS treatment. CCFM681 significantly increased goblet cells, mucin2 (MUC2), claudin-3, α-catenin1, and ZO-1, but neither CCFM760 nor CCFM642 had those protective effects. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were downregulated, while IL-10 was upregulated by CCFM681 but neither by CCFM760 nor by CCFM642. Moreover, CCFM681 treatment inhibited the toll-like receptor-4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway. Furthermore, CCFM681 treatment rebalanced gut microbiota via regulating the diversity and key microorganisms. Colonic CLA concentrations in mice fed with CCFM681 were significantly higher than that of DSS-exposed mice, while those in CCFM760 and CCFM642 groups showed insignificant difference compared with the DSS group. Moreover, CLA showed a significantly positive correlation with the effectiveness of relieving colitis. CCFM681 alleviated colitis by protecting the intestinal mechanical barrier, modulating the gut microbiota, and inhibiting the TLR4/NF-κB pathway and associated pro-inflammatory cytokines. These results will help the clinical trials of probiotics and the development of functional products for colitis.