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 Repjournal_title
Cell reportsauthors
Kovacs SB,Oh C,Maltez VI,McGlaughon BD,Verma A,Miao EA,Aachoui Ydoi
10.1016/j.celrep.2020.107967subject
Has Abstractpub_date
2020-07-28 00:00:00pages
107967issue
4issn
2211-1247pii
S2211-1247(20)30948-7journal_volume
32pub_type
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