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Pyroptosis: A Caspase-1-Dependent Programmed Cell Death and a Barrier to Infection

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The Inflammasomes

Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

Infection elicits a number of innate protective responses in the host that cooperate to promote effective pathogen clearance. Increasingly, the inflammatory response to infection appears to be coupled to cell death as an important mediator of host defence. In this chapter we review the modalities of “pyroptosis”, a highly inflammatory form of cell death mediated by the inflammasome and caspase-1 activation. Occurring in the context of infection, pyroptosis is morphologically, mechanistically and physiologically distinct from other forms of cell death. The pathogenic factors that initiate pyroptosis and the cellular mechanisms and signalling pathways responsible for its execution are examined, with a focus on the role of the inflammasome in these processes. Finally, we discuss the possible physiological significance of this unique form of cell death during infection, that is, how pyroptosis can favour pathogen elimination on one hand, while contributing to the pathophysiology of disease on the other.

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Acknowledgements

We thank Dr. Emad Alnemri, Kimmel Cancer Institute, Thomas Jefferson University for providing us with the images in Fig. 2, reproduced with permission from Nature Publishing Group, Macmillan Publishers Ltd: Labbé K, Saleh M (2008) Cell death in the host response to infection. Cell Death Differ 15(9):1339–1349, copyright 2008.

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Labbé, K., Saleh, M. (2011). Pyroptosis: A Caspase-1-Dependent Programmed Cell Death and a Barrier to Infection. In: Couillin, I., Pétrilli, V., Martinon, F. (eds) The Inflammasomes. Progress in Inflammation Research. Springer, Basel. https://doi.org/10.1007/978-3-0348-0148-5_2

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