Lactobacillus reuteri is a heterofermentative lactic acid bacterium that naturally inhabits the gut of humans and other animals. The probiotic effects of L. reuteri have been proposed to be largely associated with the production of the broad-spectrum antimicrobial compound reuterin during anaerobic metabolism of glycerol. We determined the complete genome sequences of the reuterin-producing L. reuteri JCM 1112^T and its closely related species Lactobacillus fermentum IFO 3956. Both are in the same phylogenetic group within the genus Lactobacillus. Comparative genome analysis revealed that L. reuteri JCM 1112^T has a unique cluster of 58 genes for the biosynthesis of reuterin and cobalamin (vitamin B₁₂). The 58-gene cluster has a lower GC content and is apparently inserted into the conserved region, suggesting that the cluster represents a genomic island acquired from an anomalous source. Two-dimensional nuclear magnetic resonance (2D-NMR) with ¹³C₃-glycerol demonstrated that L. reuteri JCM 1112^T could convert glycerol to reuterin in vivo, substantiating the potential of L. reuteri JCM 1112^T to produce reuterin in the intestine. Given that glycerol is shown to be naturally present in feces, the acquired ability to produce reuterin and cobalamin is an adaptive evolutionary response that likely contributes to the probiotic properties of L. reuteri.

Epithelial barrier dysfunction has been implicated as one of the major contributors to the pathogenesis of inflammatory bowel disease. The increase in intestinal permeability allows the translocation of luminal antigens across the intestinal epithelium, leading to the exacerbation of colitis. Thus, therapies targeted at specifically restoring tight junction barrier function are thought to have great potential as an alternative or supplement to immunology‐based therapies. In this study, we screened Bifidobacterium , Enterococcus, and Lactobacillus species for beneficial microbes to strengthen the intestinal epithelial barrier, using the human intestinal epithelial cell line (Caco‐2) in an in vitro assay. Some Bifidobacterium and Lactobacillus species prevented epithelial barrier disruption induced by TNF‐ α , as assessed by measuring the transepithelial electrical resistance (TER). Furthermore, live Bifidobacterium species promoted wound repair in Caco‐2 cell monolayers treated with TNF‐ α for 48 h. Time course 1H‐NMR‐based metabonomics of the culture supernatant revealed markedly enhanced production of acetate after 12 hours of coincubation of B . bifidum and Caco‐2. An increase in TER was observed by the administration of acetate to TNF‐ α ‐treated Caco‐2 monolayers. Interestingly, acetate‐induced TER‐enhancing effect in the coculture of B . bifidum and Caco‐2 cells depends on the differentiation stage of the intestinal epithelial cells. These results suggest that Bifidobacterium species enhance intestinal epithelial barrier function via metabolites such as acetate. C.‐Y. Hsieh, T. Osaka, E. Moriyama, Y. Date, J. Kikuchi, S. Tsuneda, # Strengthening of the intestinal epithelial tight junction by Bifidobacterium bifidum {#article-title-2}, Physiol Rep, 3 (3), 2015, e12327, doi: 10.14814/phy2.12327

Increasing evidence suggest that alterations of the gut microbiome underlie metabolic disease pathology by modulating gut metabolite profiles. We have shown that orally administered Porphyromonas gingivalis , a representative periodontopathic bacterium, alters the gut microbiome; that may be a novel mechanism by which periodontitis increases the risk of various diseases. Given the association between periodontal disease and metabolic diseases, it is possible that P. gingivalis can affect the metabolites. Metabolite profiling analysis demonstrated that several amino acids related to a risk of developing diabetes and obesity were elevated in P. gingivalis -administered mice. Our results revealed that the increased risk of various diseases by P. gingivalis might be mediated at least in part by alteration of metabolic profiles. The findings should add new insights into potential links between periodontal disease and systemic disease for investigators in periodontal disease and also for investigators in the field of other diseases, such as metabolic diseases.