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Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice

Environmental air pollutants including ozone cause severe lung injury and aggravate respiratory diseases such as asthma and COPD. Here we compared the effect of ozone on respiratory epithelium injury, inflammation, hyperreactivity and airway remodeling in mice upon acute (1ppm, 1 h) and chronic expo...

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Autores principales: Michaudel, Chloé, Fauconnier, Louis, Julé, Yvon, Ryffel, Bernhard
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6045627/
https://www.ncbi.nlm.nih.gov/pubmed/30006538
http://dx.doi.org/10.1038/s41598-018-28261-9
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author Michaudel, Chloé
Fauconnier, Louis
Julé, Yvon
Ryffel, Bernhard
author_facet Michaudel, Chloé
Fauconnier, Louis
Julé, Yvon
Ryffel, Bernhard
author_sort Michaudel, Chloé
collection PubMed
description Environmental air pollutants including ozone cause severe lung injury and aggravate respiratory diseases such as asthma and COPD. Here we compared the effect of ozone on respiratory epithelium injury, inflammation, hyperreactivity and airway remodeling in mice upon acute (1ppm, 1 h) and chronic exposure (1.5ppm, 2 h, twice weekly for 6 weeks). Acute ozone exposure caused respiratory epithelial disruption with protein leak and neutrophil recruitment in the broncho-alveolar space, leading to lung inflammation and airway hyperresponsiveness (AHR) to methacholine. All these parameters were increased upon chronic ozone exposure, including collagen deposition. The structure of the airways as assessed by automatic numerical image analysis showed significant differences: While acute ozone exposure increased bronchial and lumen circularity but decreased epithelial thickness and area, chronic ozone exposure revealed epithelial injury with reduced height, distended bronchioles, enlarged alveolar space and increased collagen deposition, indicative of peribronchiolar fibrosis and emphysema as characterized by a significant increase in the density and diameter of airspaces with decreased airspace numbers. In conclusion, morphometric numerical analysis enables an automatic and unbiased assessment of small airway remodeling. The structural changes of the small airways correlated with functional changes allowing to follow the progression from acute to chronic ozone induced respiratory pathology.
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spelling pubmed-60456272018-07-16 Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice Michaudel, Chloé Fauconnier, Louis Julé, Yvon Ryffel, Bernhard Sci Rep Article Environmental air pollutants including ozone cause severe lung injury and aggravate respiratory diseases such as asthma and COPD. Here we compared the effect of ozone on respiratory epithelium injury, inflammation, hyperreactivity and airway remodeling in mice upon acute (1ppm, 1 h) and chronic exposure (1.5ppm, 2 h, twice weekly for 6 weeks). Acute ozone exposure caused respiratory epithelial disruption with protein leak and neutrophil recruitment in the broncho-alveolar space, leading to lung inflammation and airway hyperresponsiveness (AHR) to methacholine. All these parameters were increased upon chronic ozone exposure, including collagen deposition. The structure of the airways as assessed by automatic numerical image analysis showed significant differences: While acute ozone exposure increased bronchial and lumen circularity but decreased epithelial thickness and area, chronic ozone exposure revealed epithelial injury with reduced height, distended bronchioles, enlarged alveolar space and increased collagen deposition, indicative of peribronchiolar fibrosis and emphysema as characterized by a significant increase in the density and diameter of airspaces with decreased airspace numbers. In conclusion, morphometric numerical analysis enables an automatic and unbiased assessment of small airway remodeling. The structural changes of the small airways correlated with functional changes allowing to follow the progression from acute to chronic ozone induced respiratory pathology. Nature Publishing Group UK 2018-07-13 /pmc/articles/PMC6045627/ /pubmed/30006538 http://dx.doi.org/10.1038/s41598-018-28261-9 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
Michaudel, Chloé
Fauconnier, Louis
Julé, Yvon
Ryffel, Bernhard
Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice
title Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice
title_full Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice
title_fullStr Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice
title_full_unstemmed Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice
title_short Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice
title_sort functional and morphological differences of the lung upon acute and chronic ozone exposure in mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6045627/
https://www.ncbi.nlm.nih.gov/pubmed/30006538
http://dx.doi.org/10.1038/s41598-018-28261-9
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