Strains producing different short-chain fatty acids alleviate DSS-induced ulcerative colitis by regulating intestinal microecology.

Probiotics have long been shown to modulate inflammatory bowel disease (IBD) in a variety of ways, and their major metabolites, short-chain fatty acids (SCFAs), have been shown to play a role in the alleviation of ulcerative colitis (UC). In the present study, DSS-treated C57BL/6J mice were gavaged with Bifidobacterium bifidum H3-R2, Propionibacterium freudenreichii B1 and Clostridium butyricum C1-6, which are capable of high production of acetic acid, propionic acid and butyric acid, respectively. We measured the effects of these three strains on inflammatory factors, intestinal barrier function, colitis-related signalling pathways, intestinal microbiome composition, and SCFA content in intestinal contents. The results of the experiment showed that all three strains differentially increased the colon length; reduced weight loss; decreased the splenic index; decreased the DAI scores and MPO activity; decreased proinflammatory factor levels (IL-8, IL-1ß and TNF-α); increased anti-inflammatory factor production (IL-10); and enhanced tight junction protein expression (ZO-1, occludin, and claudin-1). Moreover, Bifidobacterium bifidum H3-R2 and Propionibacterium freudenreichii B1 played crucial roles through TLRs/RHO kinase (ROCK1) and Wnt/ß-catenin pathways in these protective effects. In addition, three strains improved the composition of the intestinal flora and increased the production of SCFAs; notably, Propionibacterium freudenreichii B1 had the best effect. This study provides a scientific basis for the further application of probiotics in the treatment of UC in the future.

Bifidobacterium bifidum H3-R2 and Its Molecular Communication within the Context of Ulcerative Colitis.

Bifidobacteria are important mediators of immune system development within the gastrointestinal system and immunological homeostasis. The present study explored the anti-colitic activity of Bifidobacterium bifidum H3-R2 in a murine dextran sulfate sodium (DSS)-induced model of ulcerative colitis (UC). Moreover, this study offers novel insight regarding the molecular basis for the probiotic properties of B. bifidum H3-R2 by analyzing the underlying mechanisms whereby B. bifidum H3-R2-derived proteins affect the intestinal barrier. B. bifidum H3-R2 administration was sufficient to alleviate clinical manifestations consistent with DSS-induced colitis, restoring aberrant inflammatory cytokine production, enhancing tight junction protein expression, and positively impacting overall intestinal microecological homeostasis in these animals. Moreover, the bifidobacteria-derived GroEL and transaldolase (TAL) proteins were found to regulate tight junction protein expression via the NF-κB, myosin light chain kinase (MLCK), RhoA/Rho-associated protein kinase (ROCK), and mitogen-activated protein kinase (MAPK) signaling pathways, preventing the lipopolysaccharide (LPS)-mediated disruption of the intestinal epithelial cell barrier.