Figure 2.

Possible mechanisms controlled by NLRPs, VDR, and Metrnl in regulation of intestinal homeostasis and ulcerative colitis. NLRP3 and NLRP6 inflammasomes regulate secretion of IL-1β and IL-18. IL-18 helps to maintain a non-pathogenic gut microflora, which promote a healthy gut environment. IL-18 is not produced in Nlrp3^−/− or Nlrp6^−/− mice, leading to the development of potentially pathogenic species. Nlrp12^−/− mice results in a more inflammatory environment caused by higher production of cytokines such as IL-1β and IL-6. ATG16L1 is decreased in Vdr^−/− mice, which leading to reduction of AMP. Furthermore, ATG16L1 decreasing can also inhibit IL-18 production through upregulating NLRP3 expression. In the intestinal epithelial cell-specific Metrnl knockout mice, reduction of AMP leading to microbiota imbalance. NLRP, NLR family, pyrin domain-containing; VDR, vitamin D receptor; AMP, antimicrobial peptide.