Remodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection

Abstract Human rhinoviruses (HRV) are frequent cause of asthma exacerbations, however the influence of airway inflammation on the severity of viral infection is poorly understood. Here, we investigated how cytokine-induced remodeling of airway epithelium modulates antiviral response. We analyzed gen...

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Autores principales:	Bogdan Jakiela, Ana Rebane, Jerzy Soja, Stanislawa Bazan-Socha, Anet Laanesoo, Hanna Plutecka, Marcin Surmiak, Marek Sanak, Krzysztof Sladek, Grazyna Bochenek
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c31fe97f5d2f41c58b8b2cbffae50630
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spelling	oai:doaj.org-article:c31fe97f5d2f41c58b8b2cbffae506302021-12-02T17:41:27ZRemodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection10.1038/s41598-021-92252-62045-2322https://doaj.org/article/c31fe97f5d2f41c58b8b2cbffae506302021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92252-6https://doaj.org/toc/2045-2322Abstract Human rhinoviruses (HRV) are frequent cause of asthma exacerbations, however the influence of airway inflammation on the severity of viral infection is poorly understood. Here, we investigated how cytokine-induced remodeling of airway epithelium modulates antiviral response. We analyzed gene expression response in in vitro differentiated bronchial epithelium exposed to cytokines and next infected with HRV16. IL-13-induced mucous cell metaplasia (MCM) was associated with impaired ciliogenesis and induction of antiviral genes, resulting in lower susceptibility to HRV. Epithelial-mesenchymal transition caused by TGF-β was associated with increased virus replication and boosted innate response. Moreover, HRV infection per se caused transient upregulation of MCM markers and growth factors, followed by low-level virus replication and shedding. Our data suggest that the outcome of HRV infection depends on the type of lower airway inflammation and the extent of epithelial damage. Type-2 inflammation (eosinophilic asthma) may induce antiviral state of epithelium and decrease virus sensitivity, while growth factor exposure during epithelial repair may facilitate virus replication and inflammatory response. Additionally, responses to HRV were similar in cells obtained from asthma patients and control subjects, which implicates that antiviral mechanisms are not intrinsically impaired in asthma, but may develop in the presence of uncontrolled airway inflammation.Bogdan JakielaAna RebaneJerzy SojaStanislawa Bazan-SochaAnet LaanesooHanna PluteckaMarcin SurmiakMarek SanakKrzysztof SladekGrazyna BochenekNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Bogdan Jakiela Ana Rebane Jerzy Soja Stanislawa Bazan-Socha Anet Laanesoo Hanna Plutecka Marcin Surmiak Marek Sanak Krzysztof Sladek Grazyna Bochenek Remodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection
description	Abstract Human rhinoviruses (HRV) are frequent cause of asthma exacerbations, however the influence of airway inflammation on the severity of viral infection is poorly understood. Here, we investigated how cytokine-induced remodeling of airway epithelium modulates antiviral response. We analyzed gene expression response in in vitro differentiated bronchial epithelium exposed to cytokines and next infected with HRV16. IL-13-induced mucous cell metaplasia (MCM) was associated with impaired ciliogenesis and induction of antiviral genes, resulting in lower susceptibility to HRV. Epithelial-mesenchymal transition caused by TGF-β was associated with increased virus replication and boosted innate response. Moreover, HRV infection per se caused transient upregulation of MCM markers and growth factors, followed by low-level virus replication and shedding. Our data suggest that the outcome of HRV infection depends on the type of lower airway inflammation and the extent of epithelial damage. Type-2 inflammation (eosinophilic asthma) may induce antiviral state of epithelium and decrease virus sensitivity, while growth factor exposure during epithelial repair may facilitate virus replication and inflammatory response. Additionally, responses to HRV were similar in cells obtained from asthma patients and control subjects, which implicates that antiviral mechanisms are not intrinsically impaired in asthma, but may develop in the presence of uncontrolled airway inflammation.
format	article
author	Bogdan Jakiela Ana Rebane Jerzy Soja Stanislawa Bazan-Socha Anet Laanesoo Hanna Plutecka Marcin Surmiak Marek Sanak Krzysztof Sladek Grazyna Bochenek
author_facet	Bogdan Jakiela Ana Rebane Jerzy Soja Stanislawa Bazan-Socha Anet Laanesoo Hanna Plutecka Marcin Surmiak Marek Sanak Krzysztof Sladek Grazyna Bochenek
author_sort	Bogdan Jakiela
title	Remodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection
title_short	Remodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection
title_full	Remodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection
title_fullStr	Remodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection
title_full_unstemmed	Remodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection
title_sort	remodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/c31fe97f5d2f41c58b8b2cbffae50630
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Remodeling of bronchial epithelium caused by asthmatic inflammation affects its response to rhinovirus infection

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