Abstract
Leukotrienes (LTs) are potent bioactive lipid mediators whose synthesis is increased in response to inflammatory stimuli. LTB4 and the cysteinyl LTs (LTC4, LTD4 and LTE4) are products of the 5-lipoxygenase pathway of arachidonic acid metabolism and exert their biological effects through specific receptors located on the surface of target cells. In addition to promoting the recruitment and retention of inflammatory cell in the lung, LTs increase mucous secretion, enhance vascular permeability and cause airway constriction. Genetic and pharmacologic manipulation of LT biosynthetic and signaling pathways in experimental animals has uncovered a variety of functions of LTs in models of respiratory disease including allergen-induced airway inflammation and hyperresponsiveness, pulmonary fibrosis and cancer. Clinical data, including increased bronchoalveolar lavage fluid levels of LTs in numerous disease states, also indicate a prominent role for LTs in respiratory disease and dysfunction. While the effects of LT modifiers in many lung diseases have not been thoroughly investigated, the use of LT biosynthesis inhibitors and of cysLT receptor antagonists has proven valuable for the treatment of asthma. Continued investigation of the roles of LTs in the lung will undoubtedly yield significant advancements in the treatment of a variety of respiratory diseases.
Published Version
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