Neutrophil Caspase-11 Is Essential to Defend against a Cytosol-Invasive Bacterium.

Abstract:

:Either caspase-1 or caspase-11 can cleave gasdermin D to cause pyroptosis, eliminating intracellular replication niches. We previously showed that macrophages detect Burkholderia thailandensis via NLRC4, triggering the release of interleukin (IL)-18 and driving an essential interferon (IFN)-γ response that primes caspase-11. We now identify the IFN-γ-producing cells as a mixture of natural killer (NK) and T cells. Although both caspase-1 and caspase-11 can cleave gasdermin D in macrophages and neutrophils, we find that NLRC4-activated caspase-1 triggers pyroptosis in macrophages, but this pathway does not trigger pyroptosis in neutrophils. In contrast, caspase-11 triggers pyroptosis in both macrophages and neutrophils. This translates to an absolute requirement for caspase-11 in neutrophils during B. thailandensis infection in mice. We present an example of inflammasome sensors causing diverging outcomes in different cell types. Thus, cell fates are dictated not simply by the pathogen or inflammasome, but also by how the cell is wired to respond to detection events.

journal_name

Cell Rep

journal_title

Cell reports

authors

Kovacs SB,Oh C,Maltez VI,McGlaughon BD,Verma A,Miao EA,Aachoui Y

doi

10.1016/j.celrep.2020.107967

subject

Has Abstract

pub_date

2020-07-28 00:00:00

pages

107967

issue

4

issn

2211-1247

pii

S2211-1247(20)30948-7

journal_volume

32

pub_type

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