NLRP3: A Promising Therapeutic Target for Inflammatory Bowel Disease.

Abstract

Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, is an intestinal disease with complicated pathological mechanisms. The incidence of IBD has been increasing in recent years, which has a significant negative impact on the lives of patients. Therefore, it is particularly important to find new therapeutic targets and innovative drugs for the development of IBD. Recent studies have revealed that NLRP3 inflammatory vesicles can play an important role in maintaining intestinal homeostasis and sustaining the intestinal immune response in IBD. On the one hand, aberrant activation of NLRP3 inflammatory vesicles may cause excessive immune response by converting caspase-1, proIL-18, and proIL-1β to their active forms and releasing pro-inflammatory cytokines to stimulate the development and progression of IBD, and we can improve IBD by targeting blockade of NLRP3 activation. On the other hand, NLRP3 may also play an enter protective role by maintaining the homeostasis of the intestinal immune system. In this paper, we reviewed the activation mechanism of NLRP3 inflammasome, and the effects of NLRP3 inflammasome activation on IBD are discussed from two different perspectives: pathology and protection. At the same time, we listed the effects of direct inhibitors, indirect inhibitors, and natural inhibitors of NLRP3 inflammasome on IBD in combination with cutting-edge advances and clinical practice results, providing new targets and new ideas for the clinical treatment of IBD.