RAGE inhibition reduces acute lung injury in mice

Abstract The receptor for advanced glycation end-products (RAGE) is involved in inflammatory response during acute respiratory distress syndrome (ARDS). Growing body of evidence support strategies of RAGE inhibition in experimental lung injury, but its modalities and effects remain underinvestigated...

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Autores principales:	Raiko Blondonnet, Jules Audard, Corinne Belville, Gael Clairefond, Jean Lutz, Damien Bouvier, Laurence Roszyk, Christelle Gross, Marilyne Lavergne, Marianne Fournet, Loic Blanchon, Caroline Vachias, Christelle Damon-Soubeyrand, Vincent Sapin, Jean-Michel Constantin, Matthieu Jabaudon
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2a76f64b9a0e4661a47ba41fd1755ca4
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spelling	oai:doaj.org-article:2a76f64b9a0e4661a47ba41fd1755ca42021-12-02T12:32:25ZRAGE inhibition reduces acute lung injury in mice10.1038/s41598-017-07638-22045-2322https://doaj.org/article/2a76f64b9a0e4661a47ba41fd1755ca42017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07638-2https://doaj.org/toc/2045-2322Abstract The receptor for advanced glycation end-products (RAGE) is involved in inflammatory response during acute respiratory distress syndrome (ARDS). Growing body of evidence support strategies of RAGE inhibition in experimental lung injury, but its modalities and effects remain underinvestigated. Anesthetised C57BL/6JRj mice were divided in four groups; three of them underwent orotracheal instillation of acid and were treated with anti-RAGE monoclonal antibody (mAb) or recombinant soluble RAGE (sRAGE), acting as a decoy receptor. The fourth group served as a control. Lung injury was assessed by the analysis of blood gases, alveolar permeability, histology, AFC, and cytokines. Lung expression and distribution epithelial channels ENaC, Na,K-ATPase, and aquaporin (AQP)−5 were assessed. Treatment with either anti-RAGE mAb or sRAGE improved lung injury, arterial oxygenation and decreased alveolar inflammation in acid-injured animals. Anti-RAGE therapies were associated with restored AFC and increased lung expression of AQP-5 in alveolar cell. Blocking RAGE had potential therapeutic effects in a translational mouse model of ARDS, possibly through a decrease in alveolar type 1 epithelial cell injury as shown by restored AFC and lung AQP-5 expression. Further mechanistic studies are warranted to describe intracellular pathways that may control such effects of RAGE on lung epithelial injury and repair.Raiko BlondonnetJules AudardCorinne BelvilleGael ClairefondJean LutzDamien BouvierLaurence RoszykChristelle GrossMarilyne LavergneMarianne FournetLoic BlanchonCaroline VachiasChristelle Damon-SoubeyrandVincent SapinJean-Michel ConstantinMatthieu JabaudonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Raiko Blondonnet Jules Audard Corinne Belville Gael Clairefond Jean Lutz Damien Bouvier Laurence Roszyk Christelle Gross Marilyne Lavergne Marianne Fournet Loic Blanchon Caroline Vachias Christelle Damon-Soubeyrand Vincent Sapin Jean-Michel Constantin Matthieu Jabaudon RAGE inhibition reduces acute lung injury in mice
description	Abstract The receptor for advanced glycation end-products (RAGE) is involved in inflammatory response during acute respiratory distress syndrome (ARDS). Growing body of evidence support strategies of RAGE inhibition in experimental lung injury, but its modalities and effects remain underinvestigated. Anesthetised C57BL/6JRj mice were divided in four groups; three of them underwent orotracheal instillation of acid and were treated with anti-RAGE monoclonal antibody (mAb) or recombinant soluble RAGE (sRAGE), acting as a decoy receptor. The fourth group served as a control. Lung injury was assessed by the analysis of blood gases, alveolar permeability, histology, AFC, and cytokines. Lung expression and distribution epithelial channels ENaC, Na,K-ATPase, and aquaporin (AQP)−5 were assessed. Treatment with either anti-RAGE mAb or sRAGE improved lung injury, arterial oxygenation and decreased alveolar inflammation in acid-injured animals. Anti-RAGE therapies were associated with restored AFC and increased lung expression of AQP-5 in alveolar cell. Blocking RAGE had potential therapeutic effects in a translational mouse model of ARDS, possibly through a decrease in alveolar type 1 epithelial cell injury as shown by restored AFC and lung AQP-5 expression. Further mechanistic studies are warranted to describe intracellular pathways that may control such effects of RAGE on lung epithelial injury and repair.
format	article
author	Raiko Blondonnet Jules Audard Corinne Belville Gael Clairefond Jean Lutz Damien Bouvier Laurence Roszyk Christelle Gross Marilyne Lavergne Marianne Fournet Loic Blanchon Caroline Vachias Christelle Damon-Soubeyrand Vincent Sapin Jean-Michel Constantin Matthieu Jabaudon
author_facet	Raiko Blondonnet Jules Audard Corinne Belville Gael Clairefond Jean Lutz Damien Bouvier Laurence Roszyk Christelle Gross Marilyne Lavergne Marianne Fournet Loic Blanchon Caroline Vachias Christelle Damon-Soubeyrand Vincent Sapin Jean-Michel Constantin Matthieu Jabaudon
author_sort	Raiko Blondonnet
title	RAGE inhibition reduces acute lung injury in mice
title_short	RAGE inhibition reduces acute lung injury in mice
title_full	RAGE inhibition reduces acute lung injury in mice
title_fullStr	RAGE inhibition reduces acute lung injury in mice
title_full_unstemmed	RAGE inhibition reduces acute lung injury in mice
title_sort	rage inhibition reduces acute lung injury in mice
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/2a76f64b9a0e4661a47ba41fd1755ca4
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RAGE inhibition reduces acute lung injury in mice

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