Reduction of Eosinophilic Inflammation in the Airways

Reduction of Eosinophilic Inflammation in the AirwaysStudies have demonstrated that asthma is associated with chronic airway inflammation with recruitment of a number of inflammatory cells, including T cells and eosinophils. Although several chemical mediators are released during chronic airway inflammation, evidence strongly suggests that the cysteinyl leukotrienes (CysLTs) C4, D4, and E4 play key roles in asthma. Leukotrienes (LTs) are not stored in cells but are newly generated from arachidonic acid after cellular activation and are produced by eosinophils, mast cells, alveolar macrophages, and neutrophils. LTs are at least 1,000 times more potent as bronchoconstrictors than histamine or methacholine.
The pharmacologic actions of CysLTs include not only bronchoconstriction but also chemoattraction of eosinophils and increases in microvascular leakage and mucus secretion. Because LTs mediate many of the pathophysiologic features of asthma, they may play an important role in asthma. In fact, LTs are released in BAL fluid and urine during acute exacerbation of asthma and after allergen, cold-air, exercise, or aspirin challenge. Furthermore, several anti-LT modifiers, including CysLT1-receptor antagonists and 5-lipoxygenase inhibitors, significantly inhibited the bronchoconstriction in response to these challenges. The efficacy of CysLT1-receptor antagonists in the chronic management of asthma has been reported. Treatment of patients with asthma with CysLT1-receptor antagonists results in an improvement of respiratory function and a decrease in asthma symptoms. Furthermore, CysLT1-receptor antagonists have steroid-sparing effects and significantly decrease the frequency of episodes of acute exacerbation of asthma.

Montelukast is a potent and specific CysLT1-receptor antagonist.

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