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Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury

Transmigration and activation of neutrophils in the lung reflect key steps in the progression of acute lung injury (ALI). It is known that hydrogen sulfide (H(2)S) can limit neutrophil activation, but the respective mechanisms remain elusive. Here, we aimed to examine the underlying pathways in pulm...

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Autores principales: Faller, Simone, Hausler, Florian, Goeft, Andreas, von Itter, Marc-Nicolas André, Gyllenram, Veronica, Hoetzel, Alexander, Spassov, Sashko G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6168479/
https://www.ncbi.nlm.nih.gov/pubmed/30279441
http://dx.doi.org/10.1038/s41598-018-33101-x
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author Faller, Simone
Hausler, Florian
Goeft, Andreas
von Itter, Marc-Nicolas André
Gyllenram, Veronica
Hoetzel, Alexander
Spassov, Sashko G.
author_facet Faller, Simone
Hausler, Florian
Goeft, Andreas
von Itter, Marc-Nicolas André
Gyllenram, Veronica
Hoetzel, Alexander
Spassov, Sashko G.
author_sort Faller, Simone
collection PubMed
description Transmigration and activation of neutrophils in the lung reflect key steps in the progression of acute lung injury (ALI). It is known that hydrogen sulfide (H(2)S) can limit neutrophil activation, but the respective mechanisms remain elusive. Here, we aimed to examine the underlying pathways in pulmonary inflammation. In vivo, C57BL/6N mice received the H(2)S slow releasing compound GYY4137 prior to lipopolysaccharide (LPS) inhalation. LPS challenge led to pulmonary injury, inflammation, and neutrophil transmigration that were inhibited in response to H(2)S pretreatment. Moreover, H(2)S reduced mRNA expression of macrophage inflammatory protein-2 (MIP-2) and its receptor in lung tissue, as well as the accumulation of MIP-2 and interleukin-1β in the alveolar space. In vitro, GYY4137 did not exert toxic effects on Hoxb8 neutrophils, but prevented their transmigration through an endothelial barrier in the presence and absence of MIP-2. In addition, the release of MIP-2 and reactive oxygen species from LPS-stimulated Hoxb8 neutrophils were directly inhibited by H(2)S. Taken together, we provide first evidence that H(2)S limits lung neutrophil sequestration upon LPS challenge. As proposed underlying mechanisms, H(2)S prevents neutrophil transmigration through the inflamed endothelium and directly inhibits pro-inflammatory as well as oxidative signalling in neutrophils. Subsequently, H(2)S pretreatment ameliorates LPS-induced ALI.
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spelling pubmed-61684792018-10-05 Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury Faller, Simone Hausler, Florian Goeft, Andreas von Itter, Marc-Nicolas André Gyllenram, Veronica Hoetzel, Alexander Spassov, Sashko G. Sci Rep Article Transmigration and activation of neutrophils in the lung reflect key steps in the progression of acute lung injury (ALI). It is known that hydrogen sulfide (H(2)S) can limit neutrophil activation, but the respective mechanisms remain elusive. Here, we aimed to examine the underlying pathways in pulmonary inflammation. In vivo, C57BL/6N mice received the H(2)S slow releasing compound GYY4137 prior to lipopolysaccharide (LPS) inhalation. LPS challenge led to pulmonary injury, inflammation, and neutrophil transmigration that were inhibited in response to H(2)S pretreatment. Moreover, H(2)S reduced mRNA expression of macrophage inflammatory protein-2 (MIP-2) and its receptor in lung tissue, as well as the accumulation of MIP-2 and interleukin-1β in the alveolar space. In vitro, GYY4137 did not exert toxic effects on Hoxb8 neutrophils, but prevented their transmigration through an endothelial barrier in the presence and absence of MIP-2. In addition, the release of MIP-2 and reactive oxygen species from LPS-stimulated Hoxb8 neutrophils were directly inhibited by H(2)S. Taken together, we provide first evidence that H(2)S limits lung neutrophil sequestration upon LPS challenge. As proposed underlying mechanisms, H(2)S prevents neutrophil transmigration through the inflamed endothelium and directly inhibits pro-inflammatory as well as oxidative signalling in neutrophils. Subsequently, H(2)S pretreatment ameliorates LPS-induced ALI. Nature Publishing Group UK 2018-10-02 /pmc/articles/PMC6168479/ /pubmed/30279441 http://dx.doi.org/10.1038/s41598-018-33101-x Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Faller, Simone
Hausler, Florian
Goeft, Andreas
von Itter, Marc-Nicolas André
Gyllenram, Veronica
Hoetzel, Alexander
Spassov, Sashko G.
Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury
title Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury
title_full Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury
title_fullStr Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury
title_full_unstemmed Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury
title_short Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury
title_sort hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6168479/
https://www.ncbi.nlm.nih.gov/pubmed/30279441
http://dx.doi.org/10.1038/s41598-018-33101-x
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