Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice.

Human rhinovirus is a key viral trigger for asthma exacerbations. To date, murine studies investigating rhinovirus-induced exacerbation of allergic airways disease have employed systemic sensitisation/intranasal challenge with ovalbumin. In this study, we combined human-rhinovirus infection with a c...

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Autores principales: Jennifer A Phan, Anthony Kicic, Luke J Berry, Lynette B Fernandes, Graeme R Zosky, Peter D Sly, Alexander N Larcombe
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Publicado: Public Library of Science (PLoS) 2014
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spelling oai:doaj.org-article:d88529ac46474f719d545ea3ec0a13252021-11-18T08:28:08ZRhinovirus exacerbates house-dust-mite induced lung disease in adult mice.1932-620310.1371/journal.pone.0092163https://doaj.org/article/d88529ac46474f719d545ea3ec0a13252014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24632596/?tool=EBIhttps://doaj.org/toc/1932-6203Human rhinovirus is a key viral trigger for asthma exacerbations. To date, murine studies investigating rhinovirus-induced exacerbation of allergic airways disease have employed systemic sensitisation/intranasal challenge with ovalbumin. In this study, we combined human-rhinovirus infection with a clinically relevant mouse model of aero-allergen exposure using house-dust-mite in an attempt to more accurately understand the links between human-rhinovirus infection and exacerbations of asthma. Adult BALB/c mice were intranasally exposed to low-dose house-dust-mite (or vehicle) daily for 10 days. On day 9, mice were inoculated with human-rhinovirus-1B (or UV-inactivated human-rhinovirus-1B). Forty-eight hours after inoculation, we assessed bronchoalveolar cellular inflammation, levels of relevant cytokines/serum antibodies, lung function and responsiveness/sensitivity to methacholine. House-dust-mite exposure did not result in a classical TH2-driven response, but was more representative of noneosinophilic asthma. However, there were significant effects of house-dust-mite exposure on most of the parameters measured including increased cellular inflammation (primarily macrophages and neutrophils), increased total IgE and house-dust-mite-specific IgG1 and increased responsiveness/sensitivity to methacholine. There were limited effects of human-rhinovirus-1B infection alone, and the combination of the two insults resulted in additive increases in neutrophil levels and lung parenchymal responses to methacholine (tissue elastance). We conclude that acute rhinovirus infection exacerbates house-dust-mite-induced lung disease in adult mice. The similarity of our results using the naturally occurring allergen house-dust-mite, to previous studies using ovalbumin, suggests that the exacerbation of allergic airways disease by rhinovirus infection could act via multiple or conserved mechanisms.Jennifer A PhanAnthony KicicLuke J BerryLynette B FernandesGraeme R ZoskyPeter D SlyAlexander N LarcombePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 3, p e92163 (2014)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Jennifer A Phan
Anthony Kicic
Luke J Berry
Lynette B Fernandes
Graeme R Zosky
Peter D Sly
Alexander N Larcombe
Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice.
description Human rhinovirus is a key viral trigger for asthma exacerbations. To date, murine studies investigating rhinovirus-induced exacerbation of allergic airways disease have employed systemic sensitisation/intranasal challenge with ovalbumin. In this study, we combined human-rhinovirus infection with a clinically relevant mouse model of aero-allergen exposure using house-dust-mite in an attempt to more accurately understand the links between human-rhinovirus infection and exacerbations of asthma. Adult BALB/c mice were intranasally exposed to low-dose house-dust-mite (or vehicle) daily for 10 days. On day 9, mice were inoculated with human-rhinovirus-1B (or UV-inactivated human-rhinovirus-1B). Forty-eight hours after inoculation, we assessed bronchoalveolar cellular inflammation, levels of relevant cytokines/serum antibodies, lung function and responsiveness/sensitivity to methacholine. House-dust-mite exposure did not result in a classical TH2-driven response, but was more representative of noneosinophilic asthma. However, there were significant effects of house-dust-mite exposure on most of the parameters measured including increased cellular inflammation (primarily macrophages and neutrophils), increased total IgE and house-dust-mite-specific IgG1 and increased responsiveness/sensitivity to methacholine. There were limited effects of human-rhinovirus-1B infection alone, and the combination of the two insults resulted in additive increases in neutrophil levels and lung parenchymal responses to methacholine (tissue elastance). We conclude that acute rhinovirus infection exacerbates house-dust-mite-induced lung disease in adult mice. The similarity of our results using the naturally occurring allergen house-dust-mite, to previous studies using ovalbumin, suggests that the exacerbation of allergic airways disease by rhinovirus infection could act via multiple or conserved mechanisms.
format article
author Jennifer A Phan
Anthony Kicic
Luke J Berry
Lynette B Fernandes
Graeme R Zosky
Peter D Sly
Alexander N Larcombe
author_facet Jennifer A Phan
Anthony Kicic
Luke J Berry
Lynette B Fernandes
Graeme R Zosky
Peter D Sly
Alexander N Larcombe
author_sort Jennifer A Phan
title Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice.
title_short Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice.
title_full Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice.
title_fullStr Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice.
title_full_unstemmed Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice.
title_sort rhinovirus exacerbates house-dust-mite induced lung disease in adult mice.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/d88529ac46474f719d545ea3ec0a1325
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