Aspirin-induced asthma as a viral disease.
A hypothesis is presented which states that aspirin-induced asthma results from chronic viral infection. This type of asthma has, indeed, a highly characteristic clinical course, reminiscent of viral upper respiratory tract infection. It is suggested that, in response to a virus, a long time after the initial exposure, specific cytotoxic lymphocytes are produced. Their activity is suppressed by prostaglandin E2 (PGE2) produced by pulmonary alveolar macrophages. Anti-cyclo-oxygenase analgesics block PGE2 production, and allow cytotoxic lymphocytes to attack and kill their target cells, i.e. the virus-affected cells of the respiratory tract. During this reaction, toxic oxygen intermediates, lysosomal enzymes and mediators are released, which precipitate attacks of asthma. These acute attacks can be prevented by avoidance of all drugs with anti-cyclo-oxygenase activity, however, asthma continues to run a protracted course because of chronic viral infection.
D001241:Aspirin / Q000009:adverse effects*; D001249:Asthma / Q000139:chemically induced / Q000209:etiology* / Q000382:microbiology; D016861:Cyclooxygenase Inhibitors; D015232:Dinoprostone; D006801:Humans; D008954:Models, Biological; D011451:Prostaglandin-Endoperoxide Synthases / Q000276:immunology; D011458:Prostaglandins E / Q000494:pharmacology; D012141:Respiratory Tract Infections / Q000150:complications* / Q000209:etiology; D013602:T-Lymphocytes, Cytotoxic / Q000187:drug effects / Q000276:immunology; D014777:Virus Diseases / Q000150:complications* / Q000276:immunology
D016861:Cyclooxygenase Inhibitors; D011458:Prostaglandins E; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; D001241:Aspirin