Abstract
Bronchial asthma is characterized by airways' inflammation and airways' hyperresponsiveness. It is unlikely that the pathophysiology of asthma and bronchial hyperresponsiveness can be explained on the basis of a single cell or a single class of mediators. Nevertheless, the possibility that leukotrienes may contribute to the pathogenesis of the inflammatory, vasoactive, and spasmogenic components of bronchial asthma is suggested by the properties of these lipid mediators, the preferential capacity of inflammatory cells to generate leukotrienes, and the presence of leukotrienes in the airways of asthmatic subjects.
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