| Summary: | The integrity of gut barrier functions is closely associated with the pathogenesis of colitis. It is speculated that <i>Lactobacillus brevis</i> Bmb6 alleviates colitis by improving the tight junction (TJ) of the inflamed intestinal epithelial layer. In the present study, the regulatory effects of <i>L. brevis</i> Bmb6 on the TJ barrier to ameliorate colitis-symptoms were investigated. Preliminary screening showed that <i>L. brevis</i> Bmb6 exhibited strong acid and bile acid tolerance, along with antioxidants and β-galactosidase activities. In a 14-day dextran sulfate sodium (DSS)-induced colitis mouse model, treatment with <i>L. brevis</i> Bmb6 significantly decreased in the disease activity index score. In addition, histological analyses showed that treatment with <i>L. brevis</i> Bmb6 protected the structural integrity of the intestinal epithelial layer and mucin-secreting goblet cells from DSS-induced damage, with only slight infiltration of immune cells. Interestingly, western blotting analyses showed that the expression of the TJ protein, zona occluden-1, was restored in Bmb6-treated mice, but not in DSS-induced mice. Consistently, the gene expression of inflammatory cytokines (tumor necrosis factor-α and interferon-γ) was also suppressed in the Bmb6-treated mice. Hence, our findings suggest that suppression of inflammatory conditions enhanced expression of TJ protein, ZO-1, or vice versa, contributing to a colitis-ameliorating effect in <i>L. brevis</i> Bmb6.
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