Kelli Boyd
Faculty Member
Last active: 3/20/2014

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

Lamkanfi M, Moreira LO, Makena P, Spierings DC, Boyd K, Murray PJ, Green DR, Kanneganti TD
Blood. 2009 113 (12): 2742-5

PMID: 19168786 · PMCID: PMC2661861 · DOI:10.1182/blood-2008-09-178038

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.

MeSH Terms (17)

Animals Apoptosis Caspase 1 Caspase 3 Caspase 7 Chemokines Cytokines Endotoxemia Endotoxins Enzyme Activation Injections, Intraperitoneal Lymphocytes Mice Mice, Inbred C57BL Mice, Knockout Specific Pathogen-Free Organisms Spleen

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