Development of a viral exacerbation model of allergic asthma

Patients with asthma tend to suffer increased asthma symptoms when they catch flu or other viral infections. However, we don?t know why this occurs or how to treat the symptoms effectively, and patients often need to increase their asthma medication or, in severe cases, be treated in hospital. We aim to develop a novel model of influenza infection in mice that are allergic to house dust mite (HDM). Our preliminary data has shown that influenza infection of HDM allergic mice increases inflammation in the lungs, and we now aim to investigate the mechanisms behind this increased inflammation and assess the impact on other asthma symptoms such as wheezing. By using this mouse model we will be able to investigate the relationships between viral infection and house dust mite exposure in order to investigate the molecules responsible for increased asthma symptoms. In addition we will be able to assess the affect of being allergic on recovery from influenza infection. Moreover we will be able to test potential novel drugs that will dampen immune responses and hopefully alleviate symptoms

Although it is well known that asthmatic patients suffer exacerbated asthma symptoms after infection with respiratory viruses the molecular mechanisms that lead to this increase in symptoms are not well characterised. We aim to develop a novel model of influenza mediated viral exacerbation of house dust mite (HDM) allergy in mice. Preliminary data has shown that influenza infection of HDM allergic mice increases cellular influx to the lung, and we now aim to characterise the effect on lung function and development of characteristic lung pathology (eosinophilia, airway remodelling) and determine the mediators in the airway tissue and airway lumen that are responsible for this heightened immune response. Using this model to investigate the temporal relationships between viral infection and allergen exposure of sensitised mice we will be able to investigate the mechanisms leading to viral exacerbation of allergic disease, as well as assess the affect of allergy on recovery from influenza infection. Moreover we will determine the role of key inflammatory mediators, TNFalpha and IL-17 in these processes.