Aspirin-intolerant asthma (AIA) is a clinical syndrome affecting 5-10% of the asthmatic population. A class of medications called cyclooxygenase (COX) inhibitors, including aspirin and indomethacin, stimulates release of large quantities of cysteinyl leukotrienes in these patients. The cysteinyl leukotrienes released in the lungs causes worsening of asthma symptoms and breathing. The overall goal of our study is to determine how and why this release of cysteinyl leukotrienes occurs in patients with aspirin-intolerant asthma. We are studying changes in lung chemicals and cells that are associated with this reaction, utilizing bronchoscopy. Bronchoscopy involves placing a thin, fiberoptic tube into the large airways of the lung to sample small pieces of lung tissue and lung fluid. In our laboratory, this tissue and fluid is analyzed to examine activity of selected inflammatory cells, namely the mast cell and eosinophil. We also measure production of chemicals involved in inflammation, including lipid mediators and cytokines. To date, we have demonstrated that COX inhibition causes release of cysteinyl leukotrienes and 15-HETE (a lipid mediator with activity in inflammation), as well as an increase in eosinophils in the lungs. These findings will help determine the importance of cysteinyl leukotrienes and other lipid mediators in asthma.
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