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Cell volume regulation modulates NLRP3 inflammasome activation

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dc.contributor.authorCompan, Vincent
dc.contributor.authorBaroja Mazo, Alberto
dc.contributor.authorLópez Castejón ∙, Gloria
dc.contributor.authorGómez, Ana I.
dc.contributor.authorAngosto, Diego
dc.contributor.authorMontero, María T.
dc.contributor.authorHerranz, Antonio S.
dc.contributor.authorBazán, Eulalia
dc.contributor.authorReimers, Diana
dc.contributor.authorMartínez Cáceres, Carlos Manuel
dc.contributor.authorMulero Méndez, Victoriano Francisco
dc.contributor.authorPelegrín Vivancos, Pablo
dc.contributor.departmentAnatomía y Anatomía Patológica Comparadas
dc.date.accessioned2025-01-17T13:00:08Z
dc.date.available2025-01-17T13:00:08Z
dc.date.issued2012-09-21
dc.description© 2012 Elsevier Inc. This document is the Submitted, Accepted, Published, version of a Published Work that appeared in final form in Immunity. To access the final edited and published work see https://doi.org/10.1016/j.immuni.2012.06.013es
dc.description.abstractCell volume regulation is a primitive response to alterations in environmental osmolarity. The NLRP3 inflammasome is a multiprotein complex that senses pathogen- and danger-associated signals. Here, we report that, from fish to mammals, the basic mechanisms of cell swelling and regulatory volume decrease (RVD) are sensed via the NLRP3 inflammasome. We found that a decrease in extracellular osmolarity induced a K+-dependent conformational change of the preassembled NLRP3-inactive inflammasome during cell swelling, followed by activation of the NLRP3 inflammasome and caspase-1, which was controlled by transient receptor potential channels during RVD. Both mechanisms were necessary for interleukin-1β processing. Increased extracellular osmolarity prevented caspase-1 activation by different known NLRP3 activators. Collectively, our data identify cell volume regulation as a basic conserved homeostatic mechanism associated with the formation of the NLRP3 inflammasome and reveal a mechanism for NLRP3 inflammasome activation.es
dc.embargo.terms1-ene-2999
dc.formatapplication/pdfes
dc.format.extent14es
dc.identifier.citationImmunity, 2012, Vol. 37, Issue 3, pp. 487- 500
dc.identifier.doihttps://doi.org/10.1016/j.immuni.2012.06.013
dc.identifier.issnPrint: 1074-7613
dc.identifier.issnElectronic: 1097-4180
dc.identifier.urihttp://hdl.handle.net/10201/148696
dc.languageenges
dc.publisherElsevieres
dc.relationThis work was supported by grants from Plan Nacional de Investigación Científica, Desarrollo, e Innovación Tecnológica 2008–2011 (PN de I+D+I 2008–2011), Instituto de Salud Carlos III, and Fondo Europeo de Desarrollo Regional (FEDER) (EMER07/049 and PI09/0120); Fundación Séneca (11922/PI/09), managed by Fundación para la Formación e Investigación Sanitarias de la Región de Murcia (FFIS); and grants from the Spanish Ministry of Science and Technology (BIO2008-01379 and BIO2011-23400) and Fundación Marcelino Botín.es
dc.relation.publisherversionhttps://www.cell.com/immunity/fulltext/S1074-7613(12)00373-1es
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccess
dc.titleCell volume regulation modulates NLRP3 inflammasome activationes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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relation.isAuthorOfPublication369f9ade-8896-4d91-84c5-e3f94a526070
relation.isAuthorOfPublication547c4c2c-d906-4e1d-ae9a-0cdb40eef6d1
relation.isAuthorOfPublication.latestForDiscoverya11bfbe4-fe50-4173-a96d-aa785375a6be
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