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Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin.

Abstract：

:The pathogenesis of Bacillus anthracis, the bacterium that causes anthrax, depends on secretion of three factors that combine to form two bipartite toxins. Edema toxin, consisting of protective antigen (PA) and edema factor (EF), causes the edema associated with cutaneous anthrax infections, whereas lethal toxin (LeTx), consisting of PA and lethal factor (LF), is believed to be responsible for causing death in systemic anthrax infections. EF and LF can be transported by PA into the cytosol of many cell types. In mouse macrophages, LF can cause rapid necrosis that may be related to the pathology of systemic infections. Inbred mouse strains display variable sensitivity to LeTx-induced macrophage necrosis. This trait difference has been mapped to a locus on chromosome 11 named Ltxs1 (refs. 7,8). Here we show that an extremely polymorphic gene in this locus, Nalp1b, is the primary mediator of mouse macrophage susceptibility to LeTx. We also show that LeTx-induced macrophage death requires caspase-1, which is activated in susceptible, but not resistant, macrophages after intoxication, suggesting that Nalp1b directly or indirectly activates caspase-1 in response to LeTx.

journal_name

Nat Genet

journal_title

Nature genetics

authors

Boyden ED,Dietrich WF

doi

10.1038/ng1724

keywords:

subject

Has Abstract

pub_date

2006-02-01 00:00:00

pages

240-4

issue

2

eissn

1061-4036

issn

1546-1718

pii

ng1724

journal_volume

38

pub_type

杂志文章

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