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Critical role of aquaporins in IL-1β-mediated inflammation


Rabolli, Virginie; Wallemme, Laurent; Lo Re, Sandra; Uwambayinema, Francine; Palmai-Pallag, Mihaly; Thomassen, Leen; Tyteca, Donatienne; Octave, Jean-Noel; Marbaix, Etienne; Lison, Dominique; Devuyst, Olivier; Huaux, François (2014). Critical role of aquaporins in IL-1β-mediated inflammation. Journal of Biological Chemistry, 289(20):13937-13947.

Abstract

Rapid changes in cell volume characterize macrophage activation but the role of water channels in inflammation remains unclear. We show here that in vitro, AQP blockade or deficiency results in reduced IL-1β release by macrophages activated with a variety of NLRP3 stimuli. Inhibition of AQP specifically during the regulatory volume decrease process is sufficient to limit IL-1β release by macrophages through the NLRP3 inflammasome axis. The immune-related activity of AQP was confirmed in vivo in a model of acute lung inflammation induced by crystals. AQP1 deficiency is associated with a marked reduction of both lung IL-1β release and neutrophilic inflammation. We conclude that AQP-mediated water transport in macrophages constitutes a general danger signal required for NLRP3-related inflammation. Our findings reveal a new function of AQP in the inflammatory process and suggest a novel therapeutic target for anti-inflammatory therapy.

Abstract

Rapid changes in cell volume characterize macrophage activation but the role of water channels in inflammation remains unclear. We show here that in vitro, AQP blockade or deficiency results in reduced IL-1β release by macrophages activated with a variety of NLRP3 stimuli. Inhibition of AQP specifically during the regulatory volume decrease process is sufficient to limit IL-1β release by macrophages through the NLRP3 inflammasome axis. The immune-related activity of AQP was confirmed in vivo in a model of acute lung inflammation induced by crystals. AQP1 deficiency is associated with a marked reduction of both lung IL-1β release and neutrophilic inflammation. We conclude that AQP-mediated water transport in macrophages constitutes a general danger signal required for NLRP3-related inflammation. Our findings reveal a new function of AQP in the inflammatory process and suggest a novel therapeutic target for anti-inflammatory therapy.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology

04 Faculty of Medicine > Center for Integrative Human Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2014
Deposited On:09 Jul 2014 15:20
Last Modified:08 Dec 2017 06:23
Publisher:American Society for Biochemistry and Molecular Biology
ISSN:0021-9258
Additional Information:This research was originally published in Rabolli, Virginie; Wallemme, Laurent; Lo Re, Sandra; Uwambayinema, Francine; Palmai-Pallag, Mihaly; Thomassen, Leen; Tyteca, Donatienne; Octave, Jean-Noel; Marbaix, Etienne; Lison, Dominique; Devuyst, Olivier; Huaux, François (2014). Critical role of aquaporins in IL-1β-mediated inflammation. Journal of Biological Chemistry, 289(20):13937-13947. © the American Society for Biochemistry and Molecular Biology.
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1074/jbc.M113.534594
PubMed ID:24700466

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