Abstract
Methods In the acute asthma model, mice were sensitised intranasally with HDM or PBS on three consecutive days and challenged two weeks later. Two days after the challenge the mice were infected intranasally with 10 TCID50 influenza (A/PR/8/34) or PBS and sacrificed 4, 8 or 14 days after infection. In the chronic asthma model the mice receive influenza in the 5th week of sensitisation (intranasally, 5 days a week for 5 weeks). In both models we assess(ed) cellular influx by analysing bronchoalveolar lavage fluid (BALF), and cytokines and viral load in lung lysate. PenH is determined as a measure of airway hyperresponsiveness (AHR).
Highlights
Rationale Viral airway infections account for the majority of asthma exacerbations
The underlying mechanisms leading to these viral exacerbations are still not well understood. In both an acute and a chronic ‘asthma’ model using house dust mite (HDM), we investigate the effect of an influenza infection on the inflammatory response
In the acute asthma model there was a significantly higher influx of eosinophils into the lungs of the HDMtreated mice compared to the HDM/PBS and the PBS/ influenza group
Summary
Rationale Viral airway infections account for the majority of asthma exacerbations. The underlying mechanisms leading to these viral exacerbations are still not well understood. In both an acute and a chronic ‘asthma’ model using house dust mite (HDM), we investigate the effect of an influenza infection on the inflammatory response
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