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RIP Kinase-dependent necrosis drives lethal systemic inflammatory response syndrome

Linde Duprez UGent, Nozomi Takahashi UGent, Filip Van Hauwermeiren UGent, Benjamin Vandendriessche UGent, Vera Goossens UGent, Tom Vanden Berghe UGent, Wim Declercq UGent, Claude Libert UGent, Anje Cauwels UGent and Peter Vandenabeele UGent (2011) IMMUNITY. 35(6). p.908-918
abstract
Engagement of tumor necrosis factor receptor 1 signals two diametrically opposed pathways: survival-inflammation and cell death. An additional switch decides, depending on the cellular context, between caspase-dependent apoptosis and RIP kinase (RIPK)-mediated necrosis, also termed necroptosis. We explored the contribution of both cell death pathways in TNF-induced systemic inflammatory response syndrome (SIRS). Deletion of apoptotic executioner caspases (caspase-3 or -7) or inflammatory caspase-1 had no impact on lethal SIRS. However, deletion of RIPK3 conferred complete protection against lethal SIRS and reduced the amounts of circulating damage-associated molecular patterns. Pretreatment with the RIPK1 kinase inhibitor, necrostatin-1, provided a similar effect. These results suggest that RIPK1-RIPK3-mediated cellular damage by necrosis drives mortality during TNF-induced SIRS. RIPK3 deficiency also protected against cecal ligation and puncture, underscoring the clinical relevance of RIPK kinase inhibition in sepsis and identifying components of the necroptotic pathway that are potential therapeutic targets for treatment of SIRS and sepsis.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
CECAL LIGATION, STERILE INFLAMMATION, TNF-ALPHA, CELL-DEATH PATHWAY, KAPPA-B ACTIVATION, INDUCED SHOCK, RECEPTOR, APOPTOSIS, SEPSIS, PROTEIN
journal title
IMMUNITY
Immunity
volume
35
issue
6
pages
908 - 918
Web of Science type
Article
Web of Science id
000298777300010
JCR category
IMMUNOLOGY
JCR impact factor
21.637 (2011)
JCR rank
4/138 (2011)
JCR quartile
1 (2011)
ISSN
1074-7613
DOI
10.1016/j.immuni.2011.09.020
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2015324
handle
http://hdl.handle.net/1854/LU-2015324
date created
2012-02-02 09:35:09
date last changed
2013-02-27 09:09:30
@article{2015324,
  abstract     = {Engagement of tumor necrosis factor receptor 1 signals two diametrically opposed pathways: survival-inflammation and cell death. An additional switch decides, depending on the cellular context, between caspase-dependent apoptosis and RIP kinase (RIPK)-mediated necrosis, also termed necroptosis. We explored the contribution of both cell death pathways in TNF-induced systemic inflammatory response syndrome (SIRS). Deletion of apoptotic executioner caspases (caspase-3 or -7) or inflammatory caspase-1 had no impact on lethal SIRS. However, deletion of RIPK3 conferred complete protection against lethal SIRS and reduced the amounts of circulating damage-associated molecular patterns. Pretreatment with the RIPK1 kinase inhibitor, necrostatin-1, provided a similar effect. These results suggest that RIPK1-RIPK3-mediated cellular damage by necrosis drives mortality during TNF-induced SIRS. RIPK3 deficiency also protected against cecal ligation and puncture, underscoring the clinical relevance of RIPK kinase inhibition in sepsis and identifying components of the necroptotic pathway that are potential therapeutic targets for treatment of SIRS and sepsis.},
  author       = {Duprez, Linde and Takahashi, Nozomi and Van Hauwermeiren, Filip and Vandendriessche, Benjamin and Goossens, Vera and Vanden Berghe, Tom and Declercq, Wim and Libert, Claude and Cauwels, Anje and Vandenabeele, Peter},
  issn         = {1074-7613},
  journal      = {IMMUNITY},
  keyword      = {CECAL LIGATION,STERILE INFLAMMATION,TNF-ALPHA,CELL-DEATH PATHWAY,KAPPA-B ACTIVATION,INDUCED SHOCK,RECEPTOR,APOPTOSIS,SEPSIS,PROTEIN},
  language     = {eng},
  number       = {6},
  pages        = {908--918},
  title        = {RIP Kinase-dependent necrosis drives lethal systemic inflammatory response syndrome},
  url          = {http://dx.doi.org/10.1016/j.immuni.2011.09.020},
  volume       = {35},
  year         = {2011},
}

Chicago
Duprez, Linde, Nozomi Takahashi, Filip Van Hauwermeiren, Benjamin Vandendriessche, Vera Goossens, Tom Vanden Berghe, Wim Declercq, Claude Libert, Anje Cauwels, and Peter Vandenabeele. 2011. “RIP Kinase-dependent Necrosis Drives Lethal Systemic Inflammatory Response Syndrome.” Immunity 35 (6): 908–918.
APA
Duprez, Linde, Takahashi, N., Van Hauwermeiren, F., Vandendriessche, B., Goossens, V., Vanden Berghe, T., Declercq, W., et al. (2011). RIP Kinase-dependent necrosis drives lethal systemic inflammatory response syndrome. IMMUNITY, 35(6), 908–918.
Vancouver
1.
Duprez L, Takahashi N, Van Hauwermeiren F, Vandendriessche B, Goossens V, Vanden Berghe T, et al. RIP Kinase-dependent necrosis drives lethal systemic inflammatory response syndrome. IMMUNITY. 2011;35(6):908–18.
MLA
Duprez, Linde, Nozomi Takahashi, Filip Van Hauwermeiren, et al. “RIP Kinase-dependent Necrosis Drives Lethal Systemic Inflammatory Response Syndrome.” IMMUNITY 35.6 (2011): 908–918. Print.