Inflammation and airway reactivity in asthma

The increased airway reactivity characteristic of asthma may be due to contraction of airway smooth muscle, mucus hypersecretion, edema and thickening of airway walls, and the presence of serum proteins and inflammatory cells and their products in the airways. Increased airway reactivity in asthma correlates with airway epithelial damage and is clearly related to airway inflammation, a process that most likely involves a complex interaction among mast cells, lymphocytes, eosinophils, and macrophages. Thus, although symptomatic treatment of airway narrowing is best accomplished with bronchial smooth muscle relaxants, treatment of the basic pathophysiologic defect should attempt to reduce airway inflammation. Bronchodilators (inhaled beta-agonists and, occasionally, theophylline), which do not decrease airway reactivity, are often used to treat the symptoms of patients with mild or episodic asthma; inhaled corticosteroids, which do decrease airway inflammation and reactivity, are used to treat patients with more severe symptoms. Methotrexate and cromolyn sodium may also be used, although their role in treating the underlying pathophysiology remains controversial. Identification of new agents that are as effective as corticosteroids but that do not produce their side effects would represent a major therapeutic advance for patients with asthma.