Membrane damage during Listeria monocytogenes infection triggers a caspase-7 dependent cytoprotective response.

The cysteine protease caspase-7 has an established role in the execution of apoptotic cell death, but recent findings also suggest involvement of caspase-7 during the host response to microbial infection. Caspase-7 can be cleaved by the inflammatory caspase, caspase-1, and has been implicated in pro...

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Autores principales:	Sara K B Cassidy, Jon A Hagar, Thirumala Devi Kanneganti, Luigi Franchi, Gabriel Nuñez, Mary X D O'Riordan
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/db6f67d79714482587362cf7d73f8714
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spelling	oai:doaj.org-article:db6f67d79714482587362cf7d73f87142021-11-18T06:04:14ZMembrane damage during Listeria monocytogenes infection triggers a caspase-7 dependent cytoprotective response.1553-73661553-737410.1371/journal.ppat.1002628https://doaj.org/article/db6f67d79714482587362cf7d73f87142012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22807671/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374The cysteine protease caspase-7 has an established role in the execution of apoptotic cell death, but recent findings also suggest involvement of caspase-7 during the host response to microbial infection. Caspase-7 can be cleaved by the inflammatory caspase, caspase-1, and has been implicated in processing and activation of microbial virulence factors. Thus, caspase-7 function during microbial infection may be complex, and its role in infection and immunity has yet to be fully elucidated. Here we demonstrate that caspase-7 is cleaved during cytosolic infection with the intracellular bacterial pathogen, Listeria monocytogenes. Cleavage of caspase-7 during L. monocytogenes infection did not require caspase-1 or key adaptors of the primary pathways of innate immune signaling in this infection, ASC, RIP2 and MyD88. Caspase-7 protected infected macrophages against plasma membrane damage attributable to the bacterial pore-forming toxin Listeriolysin O (LLO). LLO-mediated membrane damage could itself trigger caspase-7 cleavage, independently of infection or overt cell death. We also detected caspase-7 cleavage upon treatment with other bacterial pore-forming toxins, but not in response to detergents. Taken together, our results support a model where cleavage of caspase-7 is a consequence of toxin-mediated membrane damage, a common occurrence during infection. We propose that host activation of caspase-7 in response to pore formation represents an adaptive mechanism by which host cells can protect membrane integrity during infection.Sara K B CassidyJon A HagarThirumala Devi KannegantiLuigi FranchiGabriel NuñezMary X D O'RiordanPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 8, Iss 7, p e1002628 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Sara K B Cassidy Jon A Hagar Thirumala Devi Kanneganti Luigi Franchi Gabriel Nuñez Mary X D O'Riordan Membrane damage during Listeria monocytogenes infection triggers a caspase-7 dependent cytoprotective response.
description	The cysteine protease caspase-7 has an established role in the execution of apoptotic cell death, but recent findings also suggest involvement of caspase-7 during the host response to microbial infection. Caspase-7 can be cleaved by the inflammatory caspase, caspase-1, and has been implicated in processing and activation of microbial virulence factors. Thus, caspase-7 function during microbial infection may be complex, and its role in infection and immunity has yet to be fully elucidated. Here we demonstrate that caspase-7 is cleaved during cytosolic infection with the intracellular bacterial pathogen, Listeria monocytogenes. Cleavage of caspase-7 during L. monocytogenes infection did not require caspase-1 or key adaptors of the primary pathways of innate immune signaling in this infection, ASC, RIP2 and MyD88. Caspase-7 protected infected macrophages against plasma membrane damage attributable to the bacterial pore-forming toxin Listeriolysin O (LLO). LLO-mediated membrane damage could itself trigger caspase-7 cleavage, independently of infection or overt cell death. We also detected caspase-7 cleavage upon treatment with other bacterial pore-forming toxins, but not in response to detergents. Taken together, our results support a model where cleavage of caspase-7 is a consequence of toxin-mediated membrane damage, a common occurrence during infection. We propose that host activation of caspase-7 in response to pore formation represents an adaptive mechanism by which host cells can protect membrane integrity during infection.
format	article
author	Sara K B Cassidy Jon A Hagar Thirumala Devi Kanneganti Luigi Franchi Gabriel Nuñez Mary X D O'Riordan
author_facet	Sara K B Cassidy Jon A Hagar Thirumala Devi Kanneganti Luigi Franchi Gabriel Nuñez Mary X D O'Riordan
author_sort	Sara K B Cassidy
title	Membrane damage during Listeria monocytogenes infection triggers a caspase-7 dependent cytoprotective response.
title_short	Membrane damage during Listeria monocytogenes infection triggers a caspase-7 dependent cytoprotective response.
title_full	Membrane damage during Listeria monocytogenes infection triggers a caspase-7 dependent cytoprotective response.
title_fullStr	Membrane damage during Listeria monocytogenes infection triggers a caspase-7 dependent cytoprotective response.
title_full_unstemmed	Membrane damage during Listeria monocytogenes infection triggers a caspase-7 dependent cytoprotective response.
title_sort	membrane damage during listeria monocytogenes infection triggers a caspase-7 dependent cytoprotective response.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/db6f67d79714482587362cf7d73f8714
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Membrane damage during Listeria monocytogenes infection triggers a caspase-7 dependent cytoprotective response.

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