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Clin Sci (Lond). 2013 Jun 24. [Epub ahead of print]
Differences in Respiratory Syncytial Virus and Influenza Infection in a House Dust Mite Induced Asthma Mouse Model: Consequences for Steroid Sensitivity.
Mori H, Parker NS, Rodrigues D, Hulland K, Chappell D, Hincks JS, Bright H, Evans SM, Lamb DJ.
Abstract
A significant number of clinical asthma exacerbations are triggered by viral infection. We aimed to characterise the effect of virus infection in a house dust mite (HDM) mouse model of asthma and assess the effect of oral corticosteroids. HDM alone significantly increased eosinophils, lymphocytes, neutrophils, macrophages and a number of cytokines in bronchoalveolar lavage (BAL), all of which were sensitive to treatment with prednisolone (with the exception of neutrophils). Virus infection also induced cell infiltration and cytokines. Respiratory Syncytial Virus (RSV) infection in HDM-treated animals further increased all cell types in BAL (except eosinophils, which declined), but induced no further increase in HDM-elicited cytokines. However, whilst HDM-elicited TNF-α, IFN-γ, IL-2, IL-5 and IL-10 were sensitive to prednisolone treatment, concomitant infection with RSV blocked the sensitivity towards steroid. In contrast, influenza infection in HDM challenged animals resulted in increased BAL lymphocytes, neutrophils, IFN-γ, IL-1β, IL-4, IL-5, IL-10 and IL-12, but all were attenuated by prednisolone treatment. HDM also increased exhaled nitric oxide, which was further increased by concomitant virus infection. This increase was only partially attenuated by prednisolone. RSV infection alone increased BAL mucin. However, BAL mucin was increased in HDM animals with virus infection. Chronic HDM challenge in mice elicits a broad inflammatory response that shares many characteristics with clinical asthma. Concomitant influenza or RSV infection elicits differing inflammatory profiles that differ in their sensitivity towards steroids. This model may be suitable for the assessment of novel pharmacological interventions for asthmatic exacerbation.
PMID:
23789621
[PubMed - as supplied by publisher]
Differences in Respiratory Syncytial Virus and Influenza Infection in a House Dust Mite Induced Asthma Mouse Model: Consequences for Steroid Sensitivity.
Mori H, Parker NS, Rodrigues D, Hulland K, Chappell D, Hincks JS, Bright H, Evans SM, Lamb DJ.
Abstract
A significant number of clinical asthma exacerbations are triggered by viral infection. We aimed to characterise the effect of virus infection in a house dust mite (HDM) mouse model of asthma and assess the effect of oral corticosteroids. HDM alone significantly increased eosinophils, lymphocytes, neutrophils, macrophages and a number of cytokines in bronchoalveolar lavage (BAL), all of which were sensitive to treatment with prednisolone (with the exception of neutrophils). Virus infection also induced cell infiltration and cytokines. Respiratory Syncytial Virus (RSV) infection in HDM-treated animals further increased all cell types in BAL (except eosinophils, which declined), but induced no further increase in HDM-elicited cytokines. However, whilst HDM-elicited TNF-α, IFN-γ, IL-2, IL-5 and IL-10 were sensitive to prednisolone treatment, concomitant infection with RSV blocked the sensitivity towards steroid. In contrast, influenza infection in HDM challenged animals resulted in increased BAL lymphocytes, neutrophils, IFN-γ, IL-1β, IL-4, IL-5, IL-10 and IL-12, but all were attenuated by prednisolone treatment. HDM also increased exhaled nitric oxide, which was further increased by concomitant virus infection. This increase was only partially attenuated by prednisolone. RSV infection alone increased BAL mucin. However, BAL mucin was increased in HDM animals with virus infection. Chronic HDM challenge in mice elicits a broad inflammatory response that shares many characteristics with clinical asthma. Concomitant influenza or RSV infection elicits differing inflammatory profiles that differ in their sensitivity towards steroids. This model may be suitable for the assessment of novel pharmacological interventions for asthmatic exacerbation.
PMID:
23789621
[PubMed - as supplied by publisher]
