Publication: Cell volume regulation modulates NLRP3 inflammasome activation
Authors
Compan, Vincent ; Baroja-Mazo, Alberto ; Lopez-Castejón, Gloria ; Gomez, Ana I. ; Angosto, Diego ; Montero, María T. ; Herranz, Antonio S. ; Bazán, Eulalia ; Reimers, Diana ; Martínez Cáceres, Carlos Manuel ; Mulero Méndez, Victoriano Francisco ; Pelegrín Vivancos, Pablo
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Publisher
Cell Press
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DOI
10.1016/j.immuni.2012.06.013
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info:eu-repo/semantics/article
Description
©2012. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
This document is the Accepted 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.2012.06.013
Abstract
Cell 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 the basic mechanisms of cell swelling and regulatory volume decrease (RVD) are sensed from fish to mammals by the NLRP3 inflammasome. We found that a decrease in extracellular osmolarity induced (i) a K+-dependent conformational change of the preassembled NLRP3-inactive inflammasome during cell swelling, followed by (ii) activation of the NLRP3 inflammasome and caspase-1, which was controlled by Transient Receptor Potential (TRP) channels during RVD. Both mechanisms were necessary for interleukin-1b processing. Increased extracellular osmolarity prevented caspase-1 activation by different known NLRP3 activators. Collectively, our data place cell volume regulation as a basic conserved homeostatic mechanism associated with the formation of the NLRP3 inflammasome and provides a mechanism for NLRP3 inflammasome activation.
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Citation
Immunity, volumen 37, nº 3, año 2012, páginas 487-500.
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Este ítem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc-nd/4.0/