Some probiotics have been shown to ameliorate intestinal permeability induced by pathogens in vitro [12, 13]; whereas, others probiotic bacteria have been shown to enhance tight junction integrity between intestinal epithelial cells that are not weakened [13–15]. Existing mechanistic studies have focused on the ability of probiotics to prevent alterations to few tight junction bridging proteins in disease models, e.g. the effect of VSL#3 on dextran sodium sulphate-induced colitis in mice [16] and the effect of Lactobacillus plantarum CGMCC 1258 on Enteroinvasive E. coli ATCC

43893 (serotype O124:NM)-induced barrier disruption in vitro [17]. The effect of probiotics on tight junction proteins in a healthy intestinal barrier have not been reported, nor the effect of probiotic bacteria on epithelial cell genes involved in the whole tight junction signalling CYC202 in vitro pathway, including those encoding for bridging, plaque and dual location tight junction proteins. Alteration of tight junction

signalling in healthy humans click here is a potential mechanism that could lead to the strengthening of the intestinal barrier, resulting in limiting the ability of antigens to enter the body and potentially triggering undesirable immune responses. The hypothesis of this research was that probiotic bacteria that increase intestinal barrier function achieve this, partly, by increasing the expression of the genes involved in tight junction signalling in healthy intestinal epithelial cells. L. plantarum MB452 isolated from the probiotic product VSL#3 was chosen as the test bacterium because it has a robust, repeatable, positive effect tight junction integrity, as measured by the trans-epithelial electrical resistance (TEER) in vitro (unpublished results). VLS#3, which is a mixture of eight bacteria including L. plantarum MB452, has previously been reported to enhance tight junction integrity in vitro [18], reduce colitis in rodent models [19, 20] and improve human intestinal health TCL [21–23]. The effect of L. plantarum MB452 on intestinal epithelial cells was investigated in vitro using human colon cancer cells (Caco-2 cells), a commonly

used model of the intestinal epithelium that spontaneously form tight Elafibranor junctions between adjacent cells, and trans-epithelial electrical resistance assays, whole genome microarray analysis, and fluorescent microscopy of tight junction proteins. Results Effect of L. plantarum MB452 on TEER was dose-dependent The ability of L. plantarum MB452 to increase intestinal barrier function was investigated by determining the effect on TEER using different concentrations of L. plantarum MB452 (Figure 1). At an OD600 nm of 0.3 (7 × 107 CFU/mL) L. plantarum MB452 did not cause an increase in TEER compared to the untreated controls. At an OD600 nm of 0.6 (1.8 × 108 CFU/mL) L. plantarum MB452 caused an increase in TEER of 15-20% compared to the untreated controls at 4 and 6 hours.