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

    Access Status
    Open access via publisher
    Authors
    Phan, J.
    Kicic, Anthony
    Berry, L.
    Fernandes, L.
    Zosky, G.
    Sly, P.
    Larcombe, A.
    Date
    2014
    Type
    Journal Article
    
    Metadata
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    Citation
    Phan, J. and Kicic, A. and Berry, L. and Fernandes, L. and Zosky, G. and Sly, P. and Larcombe, A. 2014. Rhinovirus exacerbates house-dust-mite induced lung disease in adult mice. PLoS ONE. 9 (3).
    Source Title
    PLoS ONE
    DOI
    10.1371/journal.pone.0092163
    ISSN
    1932-6203
    URI
    http://hdl.handle.net/20.500.11937/63312
    Collection
    • Curtin Research Publications
    Abstract

    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 TH 2 -driven response, but was more representative of noneosinophilic asthma. However, there were significant effects of house-dustmite exposure on most of the parameters measured including increased cellular inflammation (primarily macrophages and neutrophils), increased total IgE and house-dust-mite-specific IgG 1 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. © 2014 Phan et al.

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