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.