Abstract
SUMMARYNLRP6 is a member of the NLR (nucleotide-oligomerization domain-like receptor) family of proteins that recognize pathogen-derived factors and damage-associated molecular patterns in the cytosol. The function of NLRP6 has been attributed to the maintenance of epithelial integrity and host defense against microbial infections. Under some physiological conditions, NLRP6 forms a complex with ASC and caspase-1 or caspase-11 to form an inflammasome complex cleaving pro-interleukin-1β(IL-1β) and IL-18 into their biologically active forms. Here, we summarize recent advances in the understanding of the mechanisms of activation of the NLRP6 inflammasome and discuss its relevance to human disease.
Highlights
Inflammation is a host response against microbial infections and tissue damage to limit harm to the body
We showed that infection of Nlrp6À/À mice with Citrobacter rodentium resulted in reduced caspase-1 activation and IL-18 processing (Mukherjee et al, 2020)
Our results show that Cyld deficiency resulted in severe colitis, which was associated with an increased level of NLRP6 inflammasome activity and IL-18 in the colonic mucosa
Summary
Inflammation is a host response against microbial infections and tissue damage to limit harm to the body. Emerging evidence suggests cell-type- or tissue-specific NLRP6 functions (Table 1) with a critical role for NLRP6 in host defense against microbial infection and intestinal inflammation. Hematopoietic cells Ly6Chi inflammatory monocytes and neutrophils d autophagosome formation (Wlodarska et al, 2014) d protection against colitis-associated tumorigenesis (Chen et al, 2011; Normand et al, 2011) d activates IL-18-induced TNF-a production to ameliorate intestinal inflammation (Seregin et al, 2017a) macrophages and neutrophils d suppression of TLR-induced NF-kB and MAPK signaling, decreasing production of TNF-a and IL-6, dampening inflammatory response to bacterial (L. monocytogenes, S. typhimurium, and E. coli) infection (Anand et al, 2012)
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