Review: Pharmacological treatment of airway remodeling: inhaled corticosteroids or antileukotrienes?

Chronic stable asthma is characterized by inflammation of the airway wall, with abnormal accumulation of basophils, eosinophils, lymphocytes, mast cells, macrophages, dendritic cells, and myofibroblasts. Airway inflammation is not limited to severe asthma, but is also found in mild and moderate asthma. This inflammation results in a peculiar type of lymphocytic infiltration whereby Th2 lymphocytes secrete cytokines that orchestrate cellular inflammation and promote airway hyper-responsiveness. The term "airway remodeling" in bronchial asthma refers to structural changes that occur in conjunction with, or because of, chronic airway inflammation. Airway remodeling results in alterations in the airway epithelium, lamina propria, and submucosa, leading to thickening of the airway wall. Consequences of airway remodeling in asthma include incompletely reversible airway narrowing, bronchial hyper-responsiveness, airway edema, and mucus hypersecretion; these effects may predispose subjects with asthma to exacerbations and even death due to airway obstruction. To avoid this progression, it is important to follow an adequate treatment aimed at interacting and modifying the inflammatory process. Inhaled corticosteroids remain the cornerstone of asthma management. Altough several drugs, such as ketotifen, sodium cromoglycate, sodium nedocromil, and theophylline have anti-inflammatory properties, they are less effective than corticosteroids. Antileukotrienes are a new class of anti-inflammatory drugs that interfere directly with leukotriene receptors. The aim of this brief review is to delineate the effects of inhaled corticosteroids and antileukotriene drugs on inflammation and remodeling.