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Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival

(2009) BLOOD. 113(12). p.2742-2745
Author
Organization
Abstract
Abstract: Extensive apoptosis of leukocytes during sepsis and endotoxic shock constitutes an important mechanism linked to the excessive mortality associated with these disorders. Caspase inhibitors confer protection from endotoxin-induced lymphocyte apoptosis and improve survival, but it is not clear which caspases mediate lipopolysaccharide (LPS)-induced lymphocyte apoptosis and mortality. We report here that the apoptotic executioner caspase-7 was activated in the splenocytes of LPS-injected mice, suggesting a role for caspase-7 in lymphocyte apoptosis. Indeed, caspase-7-deficient mice were resistant to LPS-induced lymphocyte apoptosis and were markedly protected from LPS-induced lethality independently of the excessive production of serum cytokines. These results reveal for the first time a nonredundant role for caspase-7 in vivo and identify caspase-7 inhibition as a component of the mechanism by which caspase inhibitors protect from endotoxin-induced mortality. (Blood. 2009;113:2742-2745)
Keywords
INTERLEUKIN-1-BETA, DYSFUNCTION, SEPTIC SHOCK, DISTINCT, MICE DEFICIENT, CELL-DEATH, SEPSIS, THERAPY, ENZYME

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Chicago
Lamkanfi, Mohamed, LO Moreira, P Makena, DCJ Spierings, K Boyd, PJ Murray, DR Green, and TD Kanneganti. 2009. “Caspase-7 Deficiency Protects from Endotoxin-induced Lymphocyte Apoptosis and Improves Survival.” Blood 113 (12): 2742–2745.
APA
Lamkanfi, M., Moreira, L., Makena, P., Spierings, D., Boyd, K., Murray, P., Green, D., et al. (2009). Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival. BLOOD, 113(12), 2742–2745.
Vancouver
1.
Lamkanfi M, Moreira L, Makena P, Spierings D, Boyd K, Murray P, et al. Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival. BLOOD. WASHINGTON: AMER SOC HEMATOLOGY; 2009;113(12):2742–5.
MLA
Lamkanfi, Mohamed et al. “Caspase-7 Deficiency Protects from Endotoxin-induced Lymphocyte Apoptosis and Improves Survival.” BLOOD 113.12 (2009): 2742–2745. Print.
@article{783744,
  abstract     = {Abstract: Extensive apoptosis of leukocytes during sepsis and endotoxic shock constitutes an important mechanism linked to the excessive mortality associated with these disorders. Caspase inhibitors confer protection from endotoxin-induced lymphocyte apoptosis and improve survival, but it is not clear which caspases mediate lipopolysaccharide (LPS)-induced lymphocyte apoptosis and mortality. We report here that the apoptotic executioner caspase-7 was activated in the splenocytes of LPS-injected mice, suggesting a role for caspase-7 in lymphocyte apoptosis. Indeed, caspase-7-deficient mice were resistant to LPS-induced lymphocyte apoptosis and were markedly protected from LPS-induced lethality independently of the excessive production of serum cytokines. These results reveal for the first time a nonredundant role for caspase-7 in vivo and identify caspase-7 inhibition as a component of the mechanism by which caspase inhibitors protect from endotoxin-induced mortality. (Blood. 2009;113:2742-2745)},
  author       = {Lamkanfi, Mohamed and Moreira, LO and Makena, P and Spierings, DCJ and Boyd, K and Murray, PJ and Green, DR and Kanneganti, TD},
  issn         = {0006-4971},
  journal      = {BLOOD},
  keywords     = {INTERLEUKIN-1-BETA,DYSFUNCTION,SEPTIC SHOCK,DISTINCT,MICE DEFICIENT,CELL-DEATH,SEPSIS,THERAPY,ENZYME},
  language     = {eng},
  number       = {12},
  pages        = {2742--2745},
  publisher    = {AMER SOC HEMATOLOGY},
  title        = {Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival},
  url          = {http://dx.doi.org/10.1182/blood-2008-09-178038},
  volume       = {113},
  year         = {2009},
}

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