Distinct licensing of IL-18 and IL-1β secretion in response to NLRP3 inflammasome activation.

Inflammasome activation permits processing of interleukins (IL)-1β and 18 and elicits cell death (pyroptosis). Whether these responses are independently licensed or are "hard-wired" consequences of caspase-1 (casp1) activity has not been clear. Here, we show that that each of these respons...

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Autores principales:	Rebecca L Schmidt, Laurel L Lenz
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/02e6d419abd14e099be3524052466c63
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spelling	oai:doaj.org-article:02e6d419abd14e099be3524052466c632021-11-18T07:05:11ZDistinct licensing of IL-18 and IL-1β secretion in response to NLRP3 inflammasome activation.1932-620310.1371/journal.pone.0045186https://doaj.org/article/02e6d419abd14e099be3524052466c632012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23028835/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Inflammasome activation permits processing of interleukins (IL)-1β and 18 and elicits cell death (pyroptosis). Whether these responses are independently licensed or are "hard-wired" consequences of caspase-1 (casp1) activity has not been clear. Here, we show that that each of these responses is independently regulated following activation of NLRP3 inflammasomes by a "non-canonical" stimulus, the secreted Listeria monocytogenes (Lm) p60 protein. Primed murine dendritic cells (DCs) responded to p60 stimulation with reactive oxygen species (ROS) production and secretion of IL-1β and IL-18 but not pyroptosis. Inhibitors of ROS production inhibited secretion of IL-1β, but did not impair IL-18 secretion. Furthermore, DCs from caspase-11 (casp11)-deficient 129S6 mice failed to secrete IL-1β in response to p60 but were fully responsive for IL-18 secretion. These findings reveal that there are distinct licensing requirements for processing of IL-18 versus IL-1β by NLRP3 inflammasomes.Rebecca L SchmidtLaurel L LenzPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 9, p e45186 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Rebecca L Schmidt Laurel L Lenz Distinct licensing of IL-18 and IL-1β secretion in response to NLRP3 inflammasome activation.
description	Inflammasome activation permits processing of interleukins (IL)-1β and 18 and elicits cell death (pyroptosis). Whether these responses are independently licensed or are "hard-wired" consequences of caspase-1 (casp1) activity has not been clear. Here, we show that that each of these responses is independently regulated following activation of NLRP3 inflammasomes by a "non-canonical" stimulus, the secreted Listeria monocytogenes (Lm) p60 protein. Primed murine dendritic cells (DCs) responded to p60 stimulation with reactive oxygen species (ROS) production and secretion of IL-1β and IL-18 but not pyroptosis. Inhibitors of ROS production inhibited secretion of IL-1β, but did not impair IL-18 secretion. Furthermore, DCs from caspase-11 (casp11)-deficient 129S6 mice failed to secrete IL-1β in response to p60 but were fully responsive for IL-18 secretion. These findings reveal that there are distinct licensing requirements for processing of IL-18 versus IL-1β by NLRP3 inflammasomes.
format	article
author	Rebecca L Schmidt Laurel L Lenz
author_facet	Rebecca L Schmidt Laurel L Lenz
author_sort	Rebecca L Schmidt
title	Distinct licensing of IL-18 and IL-1β secretion in response to NLRP3 inflammasome activation.
title_short	Distinct licensing of IL-18 and IL-1β secretion in response to NLRP3 inflammasome activation.
title_full	Distinct licensing of IL-18 and IL-1β secretion in response to NLRP3 inflammasome activation.
title_fullStr	Distinct licensing of IL-18 and IL-1β secretion in response to NLRP3 inflammasome activation.
title_full_unstemmed	Distinct licensing of IL-18 and IL-1β secretion in response to NLRP3 inflammasome activation.
title_sort	distinct licensing of il-18 and il-1β secretion in response to nlrp3 inflammasome activation.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/02e6d419abd14e099be3524052466c63
work_keys_str_mv	AT rebeccalschmidt distinctlicensingofil18andil1bsecretioninresponsetonlrp3inflammasomeactivation AT laurelllenz distinctlicensingofil18andil1bsecretioninresponsetonlrp3inflammasomeactivation
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Distinct licensing of IL-18 and IL-1β secretion in response to NLRP3 inflammasome activation.

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