Although some bacterial strains show potential to prevent colitis, their mechanisms are not fully understood. Here, we investigated the anti-colitic mechanisms of Bifidobacterium longum subsp. infantis JCM 1222T, focusing on the relationship between interleukin (IL)-17A secreting CD4+ T cells and intestinal epithelial costimulatory molecules in mice. Oral administration of JCM 1222T to mice alleviated dextran sulfate sodium (DSS)-induced acute colitis. The expression of type 1 helper T (Th1)- and IL-17 producing helper T (Th17)-specific cytokines and transcriptional factors was suppressed by JCM 1222T treatment. Intestinal epithelial cells (IECs) from colitic mice induced IL-17A production from CD4+ T cells in a cell-cell contact-dependent manner, and this was suppressed by oral treatment with JCM 1222T. Using blocking antibodies for costimulatory molecules, we revealed that epithelial costimulatory molecules including CD80 and CD40, which were highly expressed in IECs from colitic mice, were involved in IEC-induced IL-17A response. Treatment of mice and intestinal epithelial cell line Colon-26 cells with JCM 1222T decreased the expression of CD80 and CD40. Collectively, these data indicate that JCM 1222T negatively regulate epithelial costimulatory molecules, and this effect might be attributed, at least in part, to suppression of IL-17A in DSS-induced colitis.

The bacterium Flavonifractor plautii (FP), which is found in human feces, has been reported to participate in catechin metabolism in the gut, but this bacterium's effects on immune function are unclear. We assessed the effect of oral administration of FP on the immune response in ovalbumin (OVA) -sensitized mice. We demonstrated that the FP treatment suppressed interleukin (IL)-4 in splenocytes and OVA-specific IgE production in serum from OVA-sensitized mice. Moreover, oral administration of FP augmented CD4 + CD25 + T cells and CD103 + CD11c + DCs. In animals of the FP group, the proportion of FP was increased in the mesenteric lymph nodes (MLNs), as was the proportion of Deferribacteres in the cecum. Oral administration of FP may inhibit the Th2 immune response by incorporation into the MLNs and/or by inducing changes in the gut microbiota. Thus, FP may be useful in alleviating antigen-induced Th2 immune responses.

Our previous study demonstrated that supplemental psyllium fibre increased cytoprotective heat-shock protein (Hsp) 25 levels in the intestinal cells of mice. Here, we examined the effect of psyllium fibre on colonic gene and protein expression and faecal microbiota in normal and colitic mice to improve the understanding of the preventive role of the supplement. DNA microarray analysis revealed that a 10 % psyllium fibre diet administered for 5 d up-regulated eleven extracellular matrix (ECM)-associated genes, including collagens and fibronectins, in normal mice. Acute colitis was induced using dextran sodium sulphate (DSS) in mice that were administered a pre-feeding 5 to 10 % psyllium fibre diet for 5 d. Psyllium fibre partially ameliorated or resolved the DSS-induced colon damage and inflammation characterised by body weight loss, colon shortening, increased levels of pro-inflammatory cytokines and decreased tight junction protein expression in the colon. Analysis of faecal microbiota using denaturing gradient gel electrophoresis of the PCR-amplified 16S rRNA gene demonstrated that psyllium fibre affected the colonic microbiota. Intestinal permeability was evaluated by growing intestinal Caco-2 cell monolayers on membrane filter supports coated with or without fibronectin and collagen. Cells grown on collagen and fibronectin coating showed higher transepithelial electrical resistance, indicating a strengthening of barrier integrity. Therefore, increased Hsp25 levels and modification of colonic ECM contribute to the observed psyllium-mediated protection against DSS-induced colitis. Furthermore, ECM modification appears to play a role in the strengthening of the colon barrier. In conclusion, psyllium fibre may be useful in the prevention of intestinal inflammatory diseases.

The present study investigated the antiallergic and anti-inflammatory effects of 10-hydroxy-cis-12-octadecenoic acid (HYA), a novel gut microbial metabolite of linoleic acid, in NC/Nga mice, a model of atopic dermatitis (AD). Feeding HYA decreased the plasma immunoglobulin E level and skin infiltration of mast cells with a concomitant decrease in dermatitis score. HYA feeding decreased TNF-α and increased claudin-1, a tight junction protein, levels in the mouse skin. Cytokine expression levels in the skin and intestinal Peyer's patches cells suggested that HYA improved the Th1/Th2 balance in mice. Immunoglobulin A concentration in the feces of the HYA-fed mice was approximately four times higher than that in the control mice. Finally, denaturing gradient gel electrophoresis of the PCR-amplified 16 S rRNA gene of fecal microbes indicated the modification of microbiota by HYA. Taken together, the alterations in the intestinal microbiota might be, at least in part, associated with the antiallergic effect of HYA.