The neutrophil NLRC4 inflammasome selectively promotes IL-1β maturation without pyroptosis during acute Salmonella challenge.

Details

Serval ID
serval:BIB_7CFAE04474B2
Type
Article: article from journal or magazin.
Collection
Publications
Title
The neutrophil NLRC4 inflammasome selectively promotes IL-1β maturation without pyroptosis during acute Salmonella challenge.
Journal
Cell reports
Author(s)
Chen K.W., Groß C.J., Sotomayor F.V., Stacey K.J., Tschopp J., Sweet M.J., Schroder K.
ISSN
2211-1247 (Electronic)
Publication state
Published
Issued date
24/07/2014
Peer-reviewed
Oui
Volume
8
Number
2
Pages
570-582
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
The macrophage NLRC4 inflammasome drives potent innate immune responses against Salmonella by eliciting caspase-1-dependent proinflammatory cytokine production (e.g., interleukin-1β [IL-1β]) and pyroptotic cell death. However, the potential contribution of other cell types to inflammasome-mediated host defense against Salmonella was unclear. Here, we demonstrate that neutrophils, typically viewed as cellular targets of IL-1β, themselves activate the NLRC4 inflammasome during acute Salmonella infection and are a major cell compartment for IL-1β production during acute peritoneal challenge in vivo. Importantly, unlike macrophages, neutrophils do not undergo pyroptosis upon NLRC4 inflammasome activation. The resistance of neutrophils to pyroptotic death is unique among inflammasome-signaling cells so far described and allows neutrophils to sustain IL-1β production at a site of infection without compromising the crucial inflammasome-independent antimicrobial effector functions that would be lost if neutrophils rapidly lysed upon caspase-1 activation. Inflammasome pathway modification in neutrophils thus maximizes host proinflammatory and antimicrobial responses during pathogen challenge.
Keywords
Animals, Apoptosis Regulatory Proteins/genetics, Apoptosis Regulatory Proteins/metabolism, Calcium-Binding Proteins/genetics, Calcium-Binding Proteins/metabolism, Caspase 1/genetics, Caspase 1/metabolism, Cell Death, Cells, Cultured, Humans, Immunity, Innate, Inflammasomes/metabolism, Interleukin-1beta/metabolism, Mice, Mice, Inbred C57BL, Neutrophils/immunology, Peritonitis/immunology, Salmonella Infections/immunology
Pubmed
Web of science
Open Access
Yes
Create date
22/09/2018 20:06
Last modification date
21/08/2019 5:35
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