Objective/purpose
Asthma is the most common chronic respiratory disease in children. Asthma exacerbation occurs when the airways acutely become obstructed, usually the result of airway inflammation. The Inflammation is caused by a unique mix of cells, and includes eosinophils. The majority of asthma exacerbations occur after a viral infection such as a common cold. Why asthmatic children develop such severe reactions to viruses is unclear. Our previous work suggests asthmatic patients develop severe airway obstruction because they have too many eosinophils in their airways before virus infection. The virus triggers these eosinophils to release harmful mediators and cause airway damage. We believe that in humans, it may be the mere presence of virus antigen that stimulates memory cells to activate the eosinophils. We hypothesize that memory T cell proliferation and eosinophil activation will occur in response to any airway virus for which immune memory exists, and that removal of the eosinophils will prevent airway hyperreactivity (AHR). In addition, we believe that this model is representative of virus-induced asthma exacerbation. As part of our project to develop non-invasive diagnostics using the metabolomic profile of urine through Nuclear Magnetic Resonance (NMR) spectroscopy, we are saving the urine samples from these animals. We hypothesize that there will be relevant differences between the urine profiles of each animal group, which will be applicable to humans.