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Abstract
Apoptosis, or programmed cell death, is a highly conserved cellular suicide mechanism. Apoptosis is critical to the effective resolution of inflammation, particularly in regulating the lifespan of the inflammatory neutrophil. Pathological dysregulation of neutrophil apoptosis prevents resolution of inflammation and is implicated in numerous inflammatory conditions. Similarly, subversion of this critical host defense mechanism by pathogens can prevent resolution of infection. Below, we describe the effects of different bacterial pathogens on regulation of neutrophil apoptosis and consider how re-engagement of these subverted mechanisms may facilitate the development of new strategies to combat infectious diseases.