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. 2011 Dec 12;195(6):931–942. doi: 10.1083/jcb.201108081

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© 2011 Ashida et al.

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Figure 1. — Bacteria-induced host cell death. Bacteria induce host cell death through several distinct modalities, including apoptosis, necrosis, and pyroptosis. Apoptosis is a type of noninflammatory programmed cell death that is triggered by two different pathways, the intrinsic (mitochondria-mediated) pathway and extrinsic (receptor-mediated) pathway. Apoptosis is morphologically characterized by membrane blebbing, cell shrinkage, DNA fragmentation, mitochondrial permeability, and caspase (except for caspase-1) activation. In apoptosis, bacteria are retained within apoptotic bodies and engulfed by phagocytic cells. Necrosis is characterized by membrane rupture, nuclear swelling, and the release of cellular contents and is accompanied by caspase-independent inflammation. Necrosis is triggered by ROS production or danger signals, such as lysosomal destabilization, calpain release, and depletion of ATP, that are induced upon bacterial infection or physical damage. Pyroptosis is a type of programmed cell death that is coordinated by inflammasome-mediated caspase-1 activation and accompanied by membrane rupture, DNA fragmentation, and the release of pro-inflammatory cytokines, including IL-1β and IL-18. PAMPs and DAMPs are recognized by NLR proteins, which assemble the inflammasome to activate caspase-1and trigger pyroptosis.