Abstract
Airway mucus hypersecretion is a key pathophysiological feature in many patients with asthma and chronic obstructive pulmonary disease (COPD). Consequently, it is important to develop drugs that inhibit mucus hypersecretion in these susceptible patients. Conventional therapy (anticholinergics, β2-adrenoceoptor agonists, corticosteroids, mucolytics and macrolide antibiotics) has variable efficacy in inhibiting airway mucus hypersecretion, and is less effective in COPD than in asthma. Novel pharmacotherapeutic targets are being investigated, including inhibitors of nerve activity, tachykinin antagonists, epoxygenase inducers, inhibitors of mucin exocytosis, inhibitors of mucin synthesis and goblet cell hyperplasia, inducers of goblet cell apoptosis, and purinoceptor antagonists and agonists to inhibit or hydrate secretions. However, real and theoretical differences differentiate the mucus hypersecretory phenotype in asthma from that in COPD. More information is required on these differences to identify specific therapeutic targets which, in turn, should lead to rational design of anti-hypersecretory drugs for treatment of airway mucus hypersecretion.