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Dual role of YM1+ M2 macrophages in allergic lung inflammation
Alternatively activated (M2 or YM1+) macrophages have been associated with the development of asthma but their contribution to disease initiation and progression remains unclear. To assess the therapeutic potential of modulating these M2 macrophages, we have studied inhibition of M2 polarisation dur...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5865212/ https://www.ncbi.nlm.nih.gov/pubmed/29572536 http://dx.doi.org/10.1038/s41598-018-23269-7 |
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author | Draijer, Christina Robbe, Patricia Boorsma, Carian E. Hylkema, Machteld N. Melgert, Barbro N. |
author_facet | Draijer, Christina Robbe, Patricia Boorsma, Carian E. Hylkema, Machteld N. Melgert, Barbro N. |
author_sort | Draijer, Christina |
collection | PubMed |
description | Alternatively activated (M2 or YM1+) macrophages have been associated with the development of asthma but their contribution to disease initiation and progression remains unclear. To assess the therapeutic potential of modulating these M2 macrophages, we have studied inhibition of M2 polarisation during and after development of allergic lung inflammation by treating with cynaropicrin, a galectin-3 pathway inhibitor. Mice that were treated with this inhibitor of M2 polarisation during induction of allergic inflammation developed less severe eosinophilic lung inflammation and less collagen deposition around airways, while the airway α-smooth muscle actin layer was unaffected. When we treated with cynaropicrin after induction of inflammation, eosinophilic lung inflammation and collagen deposition were also inhibited though to a lesser extent. Unexpectedly, both during and after induction of allergic inflammation, inhibition of M2 polarisation resulted in a shift towards neutrophilic inflammation. Moreover, airway hyperresponsiveness was worse in mice treated with cynaropicrin as compared to allergic mice without inhibitor. These results show that M2 macrophages are associated with remodeling and development of eosinophilic lung inflammation, but prevent development of neutrophilic lung inflammation and worsening of airway hyperresponsiveness. This study suggests that macrophages contribute to determining development of eosinophilic or neutrophilic lung inflammation in asthma. |
format | Online Article Text |
id | pubmed-5865212 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-58652122018-03-27 Dual role of YM1+ M2 macrophages in allergic lung inflammation Draijer, Christina Robbe, Patricia Boorsma, Carian E. Hylkema, Machteld N. Melgert, Barbro N. Sci Rep Article Alternatively activated (M2 or YM1+) macrophages have been associated with the development of asthma but their contribution to disease initiation and progression remains unclear. To assess the therapeutic potential of modulating these M2 macrophages, we have studied inhibition of M2 polarisation during and after development of allergic lung inflammation by treating with cynaropicrin, a galectin-3 pathway inhibitor. Mice that were treated with this inhibitor of M2 polarisation during induction of allergic inflammation developed less severe eosinophilic lung inflammation and less collagen deposition around airways, while the airway α-smooth muscle actin layer was unaffected. When we treated with cynaropicrin after induction of inflammation, eosinophilic lung inflammation and collagen deposition were also inhibited though to a lesser extent. Unexpectedly, both during and after induction of allergic inflammation, inhibition of M2 polarisation resulted in a shift towards neutrophilic inflammation. Moreover, airway hyperresponsiveness was worse in mice treated with cynaropicrin as compared to allergic mice without inhibitor. These results show that M2 macrophages are associated with remodeling and development of eosinophilic lung inflammation, but prevent development of neutrophilic lung inflammation and worsening of airway hyperresponsiveness. This study suggests that macrophages contribute to determining development of eosinophilic or neutrophilic lung inflammation in asthma. Nature Publishing Group UK 2018-03-23 /pmc/articles/PMC5865212/ /pubmed/29572536 http://dx.doi.org/10.1038/s41598-018-23269-7 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 Draijer, Christina Robbe, Patricia Boorsma, Carian E. Hylkema, Machteld N. Melgert, Barbro N. Dual role of YM1+ M2 macrophages in allergic lung inflammation |
title | Dual role of YM1+ M2 macrophages in allergic lung inflammation |
title_full | Dual role of YM1+ M2 macrophages in allergic lung inflammation |
title_fullStr | Dual role of YM1+ M2 macrophages in allergic lung inflammation |
title_full_unstemmed | Dual role of YM1+ M2 macrophages in allergic lung inflammation |
title_short | Dual role of YM1+ M2 macrophages in allergic lung inflammation |
title_sort | dual role of ym1+ m2 macrophages in allergic lung inflammation |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5865212/ https://www.ncbi.nlm.nih.gov/pubmed/29572536 http://dx.doi.org/10.1038/s41598-018-23269-7 |
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