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Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease

In chronic obstructive pulmonary disease (COPD) patients, bacterial and viral infections play a relevant role in worsening lung function and, therefore, favour disease progression. The inflammatory response to lung infections may become a specific indication of the bacterial and viral infections. We...

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Autores principales: D’Anna, Silvestro Ennio, Maniscalco, Mauro, Cappello, Francesco, Carone, Mauro, Motta, Andrea, Balbi, Bruno, Ricciardolo, Fabio L. M., Caramori, Gaetano, Di Stefano, Antonino
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7877965/
https://www.ncbi.nlm.nih.gov/pubmed/32997525
http://dx.doi.org/10.1080/07853890.2020.1831050
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author D’Anna, Silvestro Ennio
Maniscalco, Mauro
Cappello, Francesco
Carone, Mauro
Motta, Andrea
Balbi, Bruno
Ricciardolo, Fabio L. M.
Caramori, Gaetano
Di Stefano, Antonino
author_facet D’Anna, Silvestro Ennio
Maniscalco, Mauro
Cappello, Francesco
Carone, Mauro
Motta, Andrea
Balbi, Bruno
Ricciardolo, Fabio L. M.
Caramori, Gaetano
Di Stefano, Antonino
author_sort D’Anna, Silvestro Ennio
collection PubMed
description In chronic obstructive pulmonary disease (COPD) patients, bacterial and viral infections play a relevant role in worsening lung function and, therefore, favour disease progression. The inflammatory response to lung infections may become a specific indication of the bacterial and viral infections. We here review data on the bacterial–viral infections and related airways and lung parenchyma inflammation in stable and exacerbated COPD, focussing our attention on the prevalent molecular pathways in these different clinical conditions. The roles of macrophages, autophagy and NETosis are also briefly discussed in the context of lung infections in COPD. Controlling their combined response may restore a balanced lung homeostasis, reducing the risk of lung function decline. KEY MESSAGE: Bacteria and viruses can influence the responses of the innate and adaptive immune system in the lung of chronic obstructive pulmonary disease (COPD) patients. The relationship between viruses and bacterial colonization, and the consequences of the imbalance of these components can modulate the inflammatory state of the COPD lung. The complex actions involving immune trigger cells, which activate innate and cell-mediated inflammatory responses, could be responsible for the clinical consequences of irreversible airflow limitation, lung remodelling and emphysema in COPD patients.
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spelling pubmed-78779652021-03-11 Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease D’Anna, Silvestro Ennio Maniscalco, Mauro Cappello, Francesco Carone, Mauro Motta, Andrea Balbi, Bruno Ricciardolo, Fabio L. M. Caramori, Gaetano Di Stefano, Antonino Ann Med Pulmonary Medicine In chronic obstructive pulmonary disease (COPD) patients, bacterial and viral infections play a relevant role in worsening lung function and, therefore, favour disease progression. The inflammatory response to lung infections may become a specific indication of the bacterial and viral infections. We here review data on the bacterial–viral infections and related airways and lung parenchyma inflammation in stable and exacerbated COPD, focussing our attention on the prevalent molecular pathways in these different clinical conditions. The roles of macrophages, autophagy and NETosis are also briefly discussed in the context of lung infections in COPD. Controlling their combined response may restore a balanced lung homeostasis, reducing the risk of lung function decline. KEY MESSAGE: Bacteria and viruses can influence the responses of the innate and adaptive immune system in the lung of chronic obstructive pulmonary disease (COPD) patients. The relationship between viruses and bacterial colonization, and the consequences of the imbalance of these components can modulate the inflammatory state of the COPD lung. The complex actions involving immune trigger cells, which activate innate and cell-mediated inflammatory responses, could be responsible for the clinical consequences of irreversible airflow limitation, lung remodelling and emphysema in COPD patients. Taylor & Francis 2020-11-04 /pmc/articles/PMC7877965/ /pubmed/32997525 http://dx.doi.org/10.1080/07853890.2020.1831050 Text en © 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Pulmonary Medicine
D’Anna, Silvestro Ennio
Maniscalco, Mauro
Cappello, Francesco
Carone, Mauro
Motta, Andrea
Balbi, Bruno
Ricciardolo, Fabio L. M.
Caramori, Gaetano
Di Stefano, Antonino
Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease
title Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease
title_full Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease
title_fullStr Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease
title_full_unstemmed Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease
title_short Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease
title_sort bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease
topic Pulmonary Medicine
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7877965/
https://www.ncbi.nlm.nih.gov/pubmed/32997525
http://dx.doi.org/10.1080/07853890.2020.1831050
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