Possible mechanisms underlying mucus secretion in aspirin-sensitive asthma.
To study the hypersecretion of mucus in human airways, an in vitro model was developed. The effect of prostaglandins, nonsteroidal anti-inflammatory drugs, lipoxygenase products of arachidonic acid, and other mucus-stimulating and mucus-inhibiting agents was studied. The data suggest that arachidonic acid metabolized through its lipoxygenase pathway leads to the formation of potent stimulators of mucus release. Among them are the monohydroxyeicosatetraenoic acids, which are produced in large quantities by human airways, and the leukotrienes, which are generated during allergic reactions of the lung. As the lipoxygenase pathway is the only operant metabolic system available for arachidonic acid in the presence of aspirin and non-steroidal anti-inflammatory drugs--and as the nonsteroidal anti-inflammatory drugs themselves stimulate mucus production--it is possible that the mechanism responsible for mucus release in aspirin-sensitive asthmatics is the formation of these lipoxygenase products.
D001241:Aspirin / Q000009:adverse effects / Q000494:pharmacology*; D001249:Asthma / Q000139:chemically induced / Q000503:physiopathology*; D001980:Bronchi / Q000187:drug effects*; D006801:Humans; D008084:Lipoxygenase / Q000494:pharmacology; D008954:Models, Biological; D009093:Mucus / Q000187:drug effects* / Q000378:metabolism; D011453:Prostaglandins / Q000494:pharmacology
D011453:Prostaglandins; D008084:Lipoxygenase; D001241:Aspirin