Bifidobacterium longum subsp. infantis FJSYZ1M3 ameliorates DSS-induced colitis by maintaining the intestinal barrier, regulating inflammatory cytokines, and modifying gut microbiota.

B. longum subsp. infantis is a subspecies of Bifidobacterium longum, and very few strains are shown to have immunomodulatory effects. In the present study, the improvement of dextran sulphate sodium (DSS)-induced colitis by four B. longum subsp. infantis strains was compared. The results showed that B. longum subsp. infantis FJSYZ1M3 could significantly decrease disease activity index (DAI), inhibit weight loss and colon shortening, and attenuate colon tissue damage in DSS-induced colitis mice. And B. longum subsp. infantis FJSYZ1M3 intervention improved the integrity of intestinal tight junctions, relieved mucus layer damage and inhibited epithelial cell apoptosis, thereby maintaining the intestinal barrier. Additionally, B. longum subsp. infantis FJSYZ1M3 significantly affected the levels of inflammatory cytokines IL-6, IL-1ß, and IL-10 in the colon, thus relieving inflammation in colitis mice. Furthermore, B. longum subsp. infantis FJSYZ1M3 could ameliorate gut microbiota disturbance caused by DSS exposure and increase the level of butyric acid in cecal contents. In general, these findings suggested that B. longum subsp. infantis FJSYZ1M3 alleviated DSS-induced colitis by maintaining the intestinal barrier, regulating inflammatory cytokines, and modifying the gut microbiota.

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.

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.