Abstract
Inflammatory bowel disease (IBD) is characterized by chronic or recurrent inflammation of the gastrointestinal tract. Even though the current strategies to treat IBD include anti-inflammatory drugs and immune modulators, these treatments have side-effects. New strategies are, therefore, required to overcome the limitations of the therapies. In this study, we investigated the anti-colitic effects of allyl isothiocyanate (AITC), which is an active ingredient present in Wasabia japonica. The DSS-induced colitis model in the mouse was used to mimic human IBD and we observed that AITC treatment ameliorated the severity of colitis. We further studied the mechanism involved to ameliorate the colitis. To investigate the involvement of AITC on the intestinal barrier function, the effect on the intercellular tight junction was evaluated in the Caco-2 cell line while mucin expression was assessed in the LS174T cell line. AITC positively regulated tight junction proteins and mucin 2 (MUC2) against DSS-induced damage or depletion. Our data of in vivo studies were also consistent with the in vitro results. Furthermore, we observed that MUC2 increased by AITC is dependent on ERK signaling. In conclusion, we propose that AITC can be considered as a new strategy for treating IBD by modulating tight junction proteins and mucin.
Highlights
Inflammatory bowel diseases (IBD) including Crohn’s disease (CD) and ulcerative colitis (UC) are characterized by chronic or recurrent inflammation of the gastrointestinal tract [1]
The extent of early inflammation may, depend on the severity of the initial intestinal epithelial damage and barrier dysfunction attributed to dextran sodium sulfate (DSS)
Inflammation induced by the initial barrier dysfunction influences the intestinal barrier through inflammatory cytokines [9]
Summary
Inflammatory bowel diseases (IBD) including Crohn’s disease (CD) and ulcerative colitis (UC) are characterized by chronic or recurrent inflammation of the gastrointestinal tract [1]. The etiology of IBD is poorly understood, a previous study reported that its pathogenesis is related to the dysfunction of the intestinal epithelial barrier [2]. The intestinal epithelial barrier (including the intercellular tight junction and mucus layer) is selectively permeable to the intestinal contents, which prevents various antigens and microorganism from entering the host. In a pathological status of IBD, a dysfunctional intestinal epithelial barrier leads to increased intestinal permeability, which permits the passage of luminal antigens and bacteria and induces a host immune response [3]. A previous human study has reported that IBD patients have a dysfunctional intestinal epithelial barrier with increased intestinal permeability [4]. DSS disturbs the intestinal epithelial barrier function by decreasing tight junction proteins and mucin depletion [5,7,8]
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