Grant: Travel Awards - Institute Community Support

Background: During the 2009 H1N1 pandemic a disproportionately large percentage of morbidity was attributed to asthmatic patients. To date, there is little information about the immunological mechanism behind this epidemiological observation. It is widely accepted that asthma induces a type-2 mediated immune response in the lungs, characterized by the presence of immune cells such as eosinophils which are implicated in the development of this disease. We hypothesized that mice exhibiting signs of allergic asthma will have a preformed type-2 mediated response which prevents the required anti-viral immune response characterized by the signalling protein IFN-g. Methods: Using a previously validated model of allergic asthma, we sensitized mice with the allergens in house-dust mite extract (HDM) for 2 weeks, 5 days per week, followed by H1N1 infection. HDM sensitization was continued for another 5 days, and mice were sacrificed on day 8 post-viral infection. Results: HDM-sensitized mice exhibited significantly greater weight loss after viral infection compared with their saline treated counterparts. Analysis of the bronchoalveolar lavage collected from these mice revealed an increased presence of type-2 signaling proteins, namely IL-4 and IL-5. Furthermore, we observed a significant reduction in the expression of IFN-g, an important anti-viral signaling protein. Conclusion: Mice sensitized with HDM exhibit increased morbidity and mortality in response to H1N1 infection. This observation may be linked to a differential immune cell activation in the lungs of HDM-sensitized mice.