Treatment with Bifidobacterium bifidum 17 partially protects mice from Th1-driven inflammation in a chemically induced model of colitis

Probiotics have been suggested as an alternative therapeutical approach in the intervention of inflammatory disorders of the gastrointestinal tract (GIT). Application of single strains or probiotic mixtures has shown promising results in animal models and patients of inflammatory bowel disease (IBD). We recently demonstrated potent inhibitory capacity of a Bifidobacterium bifidum S17 on LPS-induced inflammatory events in cell culture models using intestinal epithelial cells and verified these anti-inflammatory effects in two mouse models of colitis. In the present study we analyze the anti-inflammatory effect of this potential probiotic strain in a chemically-induced model of colitis in C57BL/6 mice. This model is characterized by a strong type 1T helper (Th1) response resembling Crohn's disease, one of the two most prevalent forms of IBD. We performed macroscopic analysis and determined the effect of B. bifidum S17 on the cytokine balance in biopsies of the colonic mucosa. While treatment with B. bifidum S17 only had a marginal effect on weight loss, no difference was observed in the macroscopic parameters. However, a significant reduction in histology scores and the levels of pro-inflammatory cytokines interleukin 1β (IL-1β), interleukin 6 (IL-6), keratinocyte-derived chemokine (KC) and the inflammatory markers cyclooxigenase 2 (Cox-2) and myeloperoxidase (MPO) was observed. These results indicate that treatment with B. bifidum S17 is able to partially inhibit the strong Th1-driven intestinal inflammation induced in our model of colitis.

Research Highlights
► We assessed the anti-inflammatory effect of B. bifidum S17 on TNBS-induced colitis.
► B. bifidum S17 treatment significantly improved histological signs of inflammation.
► Treated animals showed significantly reduced protein levels of Cox-2 and MPO.
► Th1 cytokines (IL-1β, KC and IL-6) were significantly reduced in treated animals.