Bifidobacterium longum 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.

Abstract

This study aimed to explore the effects and differences of conjugated linoleic acid (CLA)-producing Bifidobacterium longum on the alleviation of dextran sulfate sodium (DSS)-induced colitis and to explore its patterns. Different B. longum strains were administered at 109 cfu/day 7 days before DSS treatment. B. longum CCFM681 significantly increased goblet cells, mucin2 (MUC2), claudin-3, α-catenin1, and ZO-1, but neither B. longum CCFM760 nor B. longum CCFM642 had those protective effects. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were downregulated, while IL-10 was upregulated by B. longum CCFM681 but neither by B. longum CCFM760 nor by B. longum CCFM642. Moreover, B. longum CCFM681 treatment inhibited the toll-like receptor-4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway. Furthermore, B. longum CCFM681 treatment rebalanced gut microbiota via regulating the diversity and key microorganisms. Colonic CLA concentrations in mice fed with B. longum CCFM681 were significantly higher than that of DSS-exposed mice, while those in B. longum CCFM760 and B. longum CCFM642 groups showed insignificant difference compared with the DSS group. Moreover, CLA showed a significantly positive correlation with the effectiveness of relieving colitis. B. longum 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.