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M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion
Respiratory syncytial virus (RSV) is a common childhood infection that in young infants can progress into severe bronchiolitis and pneumonia. Disease pathogenesis results from both viral mediated and host immune processes of which alveolar macrophages play an important part. Here, we investigated th...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Public Library of Science
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9560600/ https://www.ncbi.nlm.nih.gov/pubmed/36228018 http://dx.doi.org/10.1371/journal.pone.0276013 |
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author | Ronaghan, Natalie J. Soo, Mandy Pena, Uriel Tellis, Marisa Duan, Wenming Tabatabaei-Zavareh, Nooshin Kramer, Philipp Hou, Juan Moraes, Theo J. |
author_facet | Ronaghan, Natalie J. Soo, Mandy Pena, Uriel Tellis, Marisa Duan, Wenming Tabatabaei-Zavareh, Nooshin Kramer, Philipp Hou, Juan Moraes, Theo J. |
author_sort | Ronaghan, Natalie J. |
collection | PubMed |
description | Respiratory syncytial virus (RSV) is a common childhood infection that in young infants can progress into severe bronchiolitis and pneumonia. Disease pathogenesis results from both viral mediated and host immune processes of which alveolar macrophages play an important part. Here, we investigated the role of different types of alveolar macrophages on RSV infection using an in vitro co-culture model involving primary tissue-derived human bronchial epithelial cells (HBECs) and human blood monocyte-derived M0-like, M1-like, or M2-like macrophages. It was hypothesized that the in vitro model would recapitulate previous in vivo findings of a protective effect of macrophages against RSV infection. It was found that macrophages maintained their phenotype for the 72-hour co-culture time period and the bronchial epithelial cells were unaffected by the macrophage media. HBEC infection with RSV was decreased by M1-like macrophages but enhanced by M0- or M2-like macrophages. The medium used during the co-culture also impacted the outcome of the infection. This work demonstrates that alveolar macrophage phenotypes may have differential roles during epithelial RSV infection, and demonstrates that an in vitro co-culture model could be used to further investigate the roles of macrophages during bronchial viral infection. |
format | Online Article Text |
id | pubmed-9560600 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-95606002022-10-14 M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion Ronaghan, Natalie J. Soo, Mandy Pena, Uriel Tellis, Marisa Duan, Wenming Tabatabaei-Zavareh, Nooshin Kramer, Philipp Hou, Juan Moraes, Theo J. PLoS One Research Article Respiratory syncytial virus (RSV) is a common childhood infection that in young infants can progress into severe bronchiolitis and pneumonia. Disease pathogenesis results from both viral mediated and host immune processes of which alveolar macrophages play an important part. Here, we investigated the role of different types of alveolar macrophages on RSV infection using an in vitro co-culture model involving primary tissue-derived human bronchial epithelial cells (HBECs) and human blood monocyte-derived M0-like, M1-like, or M2-like macrophages. It was hypothesized that the in vitro model would recapitulate previous in vivo findings of a protective effect of macrophages against RSV infection. It was found that macrophages maintained their phenotype for the 72-hour co-culture time period and the bronchial epithelial cells were unaffected by the macrophage media. HBEC infection with RSV was decreased by M1-like macrophages but enhanced by M0- or M2-like macrophages. The medium used during the co-culture also impacted the outcome of the infection. This work demonstrates that alveolar macrophage phenotypes may have differential roles during epithelial RSV infection, and demonstrates that an in vitro co-culture model could be used to further investigate the roles of macrophages during bronchial viral infection. Public Library of Science 2022-10-13 /pmc/articles/PMC9560600/ /pubmed/36228018 http://dx.doi.org/10.1371/journal.pone.0276013 Text en © 2022 Ronaghan et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Ronaghan, Natalie J. Soo, Mandy Pena, Uriel Tellis, Marisa Duan, Wenming Tabatabaei-Zavareh, Nooshin Kramer, Philipp Hou, Juan Moraes, Theo J. M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion |
title | M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion |
title_full | M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion |
title_fullStr | M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion |
title_full_unstemmed | M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion |
title_short | M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion |
title_sort | m1-like, but not m0- or m2-like, macrophages, reduce rsv infection of primary bronchial epithelial cells in a media-dependent fashion |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9560600/ https://www.ncbi.nlm.nih.gov/pubmed/36228018 http://dx.doi.org/10.1371/journal.pone.0276013 |
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