Abstract
The integrity of gut barrier functions is closely associated with the pathogenesis of colitis. It is speculated that Lactobacillus brevis Bmb6 alleviates colitis by improving the tight junction (TJ) of the inflamed intestinal epithelial layer. In the present study, the regulatory effects of L. brevis Bmb6 on the TJ barrier to ameliorate colitis-symptoms were investigated. Preliminary screening showed that L. brevis 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 L. brevis Bmb6 significantly decreased in the disease activity index score. In addition, histological analyses showed that treatment with L. brevis 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 L. brevis Bmb6.
Highlights
Inflammatory bowel disease (IBD) is a gastrointestinal tract disorder characterized by chronic inflammation of the mucosal cells
We found that L. brevis Bmb6 regulates the cross-talk between inflammatory mediators and tight junction (TJ) protein in dextran sulfate sodium (DSS)-induced colitis mice, which in turn restores gut epithelial structural integrity and relieves colitis symptoms
Numerous studies have reported that consumption of fermented food helps in alleviating
Summary
Inflammatory bowel disease (IBD) is a gastrointestinal tract disorder characterized by chronic inflammation of the mucosal cells. It has been reported that prolonged exposure to pro-inflammatory mediators and pathogenic bacteria and viruses results in the dysregulation of TJ barrier function, subsequently leading to intestinal epithelial damage and increased paracellular permeability, as observed in IBD [8,11,12]. It was speculated that L. brevis Bmb reconstitute the integrity of the gut barrier by restoring the expression and localization of TJ proteins in the inflamed intestinal epidermal layer, thereby contributing to the colitis-ameliorating effect. The regulatory effect of Lactobacillus brevis Bmb on the expression of inflammatory factors and TJ proteins was elucidated using a DSS-induced colitis mouse model. We found that L. brevis Bmb regulates the cross-talk between inflammatory mediators and TJ protein in DSS-induced colitis mice, which in turn restores gut epithelial structural integrity and relieves colitis symptoms
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