Cell death is a fundamental biological phenomenon that is essential for the survival and development of an organism. Emerging evidence also indicates that cell death contributes to immune defense against infectious diseases. Pyroptosis is a form of inflammatory programmed cell death pathway activated by human and mouse caspase-1, human caspase-4 and caspase-5, or mouse caspase-11. These inflammatory caspases are used by the host to control bacterial, viral, fungal, or protozoan pathogens. Pyroptosis requires cleavage and activation of the pore-forming effector protein gasdermin D by inflammatory caspases. Physical rupture of the cell causes release of the pro-inflammatory cytokines IL-1β and IL-18, alarmins and endogenous danger-associated molecular patterns, signifying the inflammatory potential of pyroptosis. Here, we describe the central role of inflammatory caspases and pyroptosis in mediating immunity to infection and clearance of pathogens.
Keywords: bacteria; caspase-1; caspase-11; caspase-4; caspase-5; cell death; gasdermin D; infection; inflammasomes; inflammation; inflammatory caspases; interferons; lysis; lytic; necroptosis; necrosis; pores; pyroptosis; viruses.
© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.