Journal
CELL REPORTS
Volume 8, Issue 2, Pages 569-581Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2014.06.028
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Funding
- ANZ Trustee Medical Research Program postgraduate scholarship
- Natural Science and Engineering Research Council of Canada
- Australian Research Council Future Fellowship [FT0991576, FT100100657, FT130100361]
- National Health and Medical Research Council of Australia project [1050651]
- National Health and Medical Research Council of Australia Senior Research Fellowship [1003470]
- National Health and Medical Research Council of Australia [490993, 1023297, 1064945]
- Queensland Smart Futures Fund
- National Health and Medical Research Council of Australia [1064945] Funding Source: NHMRC
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The macrophage NLRC4 inflammasome drives potent innate immune responses against Salmonella by eliciting caspase-1-dependent proinflammatory cytokine production (e.g., interleukin-1 beta [IL-1 beta]) 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-1 beta, themselves activate the NLRC4 inflammasome during acute Salmonella infection and are a major cell compartment for IL-1 beta 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-1 beta 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.
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