TY - JOUR
T1 - The Nlrp3 inflammasome
T2 - Contributions to intestinal homeostasis
AU - Zaki, Md Hasan
AU - Lamkanfi, Mohamed
AU - Kanneganti, Thirumala Devi
N1 - Funding Information:
We acknowledge the researchers who have contributed to this field but whose work is not cited or was cited through review articles because of space limitations. This work is supported by National Institute of Health grants AR056296 and AI088177, a NIAMS Centers of Excellence for Influenza Research and Surveillance (CEIRS) grant and the American Lebanese Syrian Associated Charities (ALSAC) to T-D. K. M.L. is supported by the European Union Framework Program 7 Marie-Curie grant 256432 and by the Fonds voor Wetenschappelijk Onderzoek-Vlaanderen.
PY - 2011/4
Y1 - 2011/4
N2 - Inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis constitute a major health problem in developed countries. Moreover, IBD predisposes to the development of colorectal cancer. The intracellular NOD-like receptor Nlrp3 is rapidly emerging as a crucial regulator of intestinal homeostasis. This innate immune receptor mediates assembly of the inflammasome complex in the presence of microbial ligands, triggering caspase-1 activation and secretion of IL-1β and IL-18. Recent studies suggest that defective Nlrp3 inflammasome signaling in the gut contributes to IBD through increased permeability across the epithelial barrier and the induction of detrimental immune responses against invading commensals. Here, we review and discuss recent advances of the role of the Nlrp3 inflammasome in colitis and colon tumorigenesis.
AB - Inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis constitute a major health problem in developed countries. Moreover, IBD predisposes to the development of colorectal cancer. The intracellular NOD-like receptor Nlrp3 is rapidly emerging as a crucial regulator of intestinal homeostasis. This innate immune receptor mediates assembly of the inflammasome complex in the presence of microbial ligands, triggering caspase-1 activation and secretion of IL-1β and IL-18. Recent studies suggest that defective Nlrp3 inflammasome signaling in the gut contributes to IBD through increased permeability across the epithelial barrier and the induction of detrimental immune responses against invading commensals. Here, we review and discuss recent advances of the role of the Nlrp3 inflammasome in colitis and colon tumorigenesis.
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U2 - 10.1016/j.it.2011.02.002
DO - 10.1016/j.it.2011.02.002
M3 - Review article
C2 - 21388882
AN - SCOPUS:79953084107
SN - 1471-4906
VL - 32
SP - 171
EP - 179
JO - Trends in Immunology
JF - Trends in Immunology
IS - 4
ER -