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anthrax lethal factor cleavage of nlrp1 is required for activation of the inflammasome炭疽致死因子的乳沟nlrp1 inflammasome需要激活
Anthrax Lethal Factor Cleavage of Nlrp1 Is Required for
Activation of the Inflammasome
Jonathan L. Levinsohn., Zachary L. Newman., Kristina A. Hellmich, Rasem Fattah, Matthew A. Getz,
Shihui Liu, Inka Sastalla, Stephen H. Leppla, Mahtab Moayeri*
Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America
Abstract
NOD-like receptor (NLR) proteins (Nlrps) are cytosolic sensors responsible for detection of pathogen and danger-associated
molecular patterns through unknown mechanisms. Their activation in response to a wide range of intracellular danger
signals leads to formation of the inflammasome, caspase-1 activation, rapid programmed cell death (pyroptosis) and
maturation of IL-1b and IL-18. Anthrax lethal toxin (LT) induces the caspase-1-dependent pyroptosis of mouse and rat
macrophages isolated from certain inbred rodent strains through activation of the NOD-like receptor (NLR) Nlrp1
inflammasome. Here we show that LT cleaves rat Nlrp1 and this cleavage is required for toxin-induced inflammasome
activation, IL-1 b release, and macrophage pyroptosis. These results identify both a previously unrecognized mechanism of
activation of an NLR and a new, physiologically relevant protein substrate of LT.
Citation: Levinsohn JL, Newman ZL, Hellmich KA, Fattah R, Getz MA, et al. (2012) Anthrax Lethal Factor Cleavage of Nlrp1 Is Required for Activation of the
Inflammasome. PLoS Pathog 8(3): e1002638. doi:10.1371/journal.ppat.1002638
Editor: John A. T. Young, The Salk Institute for Biological Studies, United States of America
Received January 4, 2012; Accepted February 24, 2012; Published March 29, 2012
This is an open-access article, free of all copyright, and may be freel
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