Abstract
Airway inflammation in patients with asthma is characterized by an influx of eosinophils into the lungs, bronchial epithelial damage, mucus secretion, smooth muscle hypertrophy, and mucosal edema. The 5-lipoxygenase products of arachidonic acid termed leukotrienes are important mediators of this inflammatory response in the lungs. New modalities for the therapy of asthma are compounds that block either leukotriene formation or the actions of leukotrienes by specific receptor antagonists. The leukotriene pathway inhibitors and antagonists have demonstrated
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