140407 - does NLPR3 inflammasome.pdf (1.84 MB)
Does NLRP3 inflammasome and aryl hydrocarbon receptor play an interlinked role in bowel inflammation and colitis-associated colorectal cancer?
journal contributionposted on 2023-05-20, 16:56 authored by Ngui, IQH, Perera, AP, Rajaraman Eri
Inflammation is a hallmark in many forms of cancer; with colitis-associated colorectal cancer (CAC) being a progressive intestinal inflammation due to inflammatory bowel disease (IBD). While this is an exemplification of the negatives of inflammation, it is just as crucial to have some degree of the inflammatory process to maintain a healthy immune system. A pivotal component in the maintenance of such intestinal homeostasis is the innate immunity component, inflammasomes. Inflammasomes are large, cytosolic protein complexes formed following stimulation of microbial and stress signals that lead to the expression of pro-inflammatory cytokines. The NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome has been extensively studied in part due to its strong association with colitis and CAC. The aryl hydrocarbon receptor (AhR) has recently been acknowledged for its connection to the immune system aside from its role as an environmental sensor. AhR has been described to play a role in the inhibition of the NLRP3 inflammasome activation pathway. This review will summarise the signalling pathways of both the NLRP3 inflammasome and AhR; as well as new-found links between these two signalling pathways in intestinal immunity and some potential therapeutic agents that have been found to take advantage of this link in the treatment of colitis and CAC.
Department/SchoolTasmanian School of Medicine
PublisherMolecular Diversity Preservation International
Place of publicationMatthaeusstrasse 11, Basel, Switzerland, Ch-4057
Rights statementCopyright This is an open access article distributed under the Creative Commons Attribution 4.0 International (CC BY 4.0) License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited https://creativecommons.org/licenses/by/4.0/