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IL-18 production downstream of the Nlrp3 inflammasome confers protection against colorectal tumor formation

Mohammad Hasan Zaki, Peter Vogel, Mathilde Body-Malapel, Mohamed Lamkanfi UGent and Thirumala-Devi Kanneganti (2010) JOURNAL OF IMMUNOLOGY. 185(8). p.4912-4920
abstract
Colorectal cancer is a leading cause of cancer-related deaths worldwide. Chronic inflammation is recognized as a predisposing factor for the development of colon cancer, but the molecular mechanisms linking inflammation and tumorigenesis have remained elusive. Recent studies revealed a crucial role for the NOD-like receptor protein Nlrp3 in regulating inflammation through the assembly of proinflammatory protein complexes termed inflammasomes. However, its role in colorectal tumor formation remains unclear. In this study, we showed that mice deficient for Nlrp3 or the inflammasome effector caspase-1 were highly susceptible to azoxymethane/dextran sodium sulfate-induced inflammation and suffered from dramatically increased tumor burdens in the colon. This was a consequence of markedly reduced IL-18 levels in mice lacking components of the Nlrp3 inflammasome, which led to impaired production and activation of the tumor suppressors IFN-gamma and STAT1, respectively. Thus, IL-18 production downstream of the Nlrp3 inflammasome is critically involved in protection against colorectal tumorigenesis.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
TOLL-LIKE-RECEPTORS, GAMMA-INDUCING FACTOR, MEDIATES IFN-GAMMA, INTERFERON-GAMMA, CROHNS-DISEASE, ULCERATIVE-COLITIS, BOWEL-DISEASE, CELL LINE, JAK-STAT, KAPPA-B
journal title
JOURNAL OF IMMUNOLOGY
J. Immunol.
volume
185
issue
8
pages
4912 - 4920
Web of Science type
Article
Web of Science id
000282525900045
JCR category
IMMUNOLOGY
JCR impact factor
5.745 (2010)
JCR rank
20/133 (2010)
JCR quartile
1 (2010)
ISSN
0022-1767
DOI
10.4049/jimmunol.1002046
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1062774
handle
http://hdl.handle.net/1854/LU-1062774
date created
2010-10-22 14:54:37
date last changed
2016-12-19 15:46:27
@article{1062774,
  abstract     = {Colorectal cancer is a leading cause of cancer-related deaths worldwide. Chronic inflammation is recognized as a predisposing factor for the development of colon cancer, but the molecular mechanisms linking inflammation and tumorigenesis have remained elusive. Recent studies revealed a crucial role for the NOD-like receptor protein Nlrp3 in regulating inflammation through the assembly of proinflammatory protein complexes termed inflammasomes. However, its role in colorectal tumor formation remains unclear. In this study, we showed that mice deficient for Nlrp3 or the inflammasome effector caspase-1 were highly susceptible to azoxymethane/dextran sodium sulfate-induced inflammation and suffered from dramatically increased tumor burdens in the colon. This was a consequence of markedly reduced IL-18 levels in mice lacking components of the Nlrp3 inflammasome, which led to impaired production and activation of the tumor suppressors IFN-gamma and STAT1, respectively. Thus, IL-18 production downstream of the Nlrp3 inflammasome is critically involved in protection against colorectal tumorigenesis.},
  author       = {Zaki, Mohammad Hasan and Vogel, Peter and Body-Malapel, Mathilde and Lamkanfi, Mohamed and Kanneganti, Thirumala-Devi},
  issn         = {0022-1767},
  journal      = {JOURNAL OF IMMUNOLOGY},
  keyword      = {TOLL-LIKE-RECEPTORS,GAMMA-INDUCING FACTOR,MEDIATES IFN-GAMMA,INTERFERON-GAMMA,CROHNS-DISEASE,ULCERATIVE-COLITIS,BOWEL-DISEASE,CELL LINE,JAK-STAT,KAPPA-B},
  language     = {eng},
  number       = {8},
  pages        = {4912--4920},
  title        = {IL-18 production downstream of the Nlrp3 inflammasome confers protection against colorectal tumor formation},
  url          = {http://dx.doi.org/10.4049/jimmunol.1002046},
  volume       = {185},
  year         = {2010},
}

Chicago
Zaki, Mohammad Hasan, Peter Vogel, Mathilde Body-Malapel, Mohamed Lamkanfi, and Thirumala-Devi Kanneganti. 2010. “IL-18 Production Downstream of the Nlrp3 Inflammasome Confers Protection Against Colorectal Tumor Formation.” Journal of Immunology 185 (8): 4912–4920.
APA
Zaki, Mohammad Hasan, Vogel, P., Body-Malapel, M., Lamkanfi, M., & Kanneganti, T.-D. (2010). IL-18 production downstream of the Nlrp3 inflammasome confers protection against colorectal tumor formation. JOURNAL OF IMMUNOLOGY, 185(8), 4912–4920.
Vancouver
1.
Zaki MH, Vogel P, Body-Malapel M, Lamkanfi M, Kanneganti T-D. IL-18 production downstream of the Nlrp3 inflammasome confers protection against colorectal tumor formation. JOURNAL OF IMMUNOLOGY. 2010;185(8):4912–20.
MLA
Zaki, Mohammad Hasan, Peter Vogel, Mathilde Body-Malapel, et al. “IL-18 Production Downstream of the Nlrp3 Inflammasome Confers Protection Against Colorectal Tumor Formation.” JOURNAL OF IMMUNOLOGY 185.8 (2010): 4912–4920. Print.