Airway hypersecretion in allergic rhinitis and asthma: new pharmacotherapy.
Mucus hypersecretion is a prominent feature of allergic rhinitis and asthma. Biologic targets for suppression of hypersecretion range from the inflammatory cells that initiate airway inflammation, to specific cellular elements such as calcium-activated chloride (CLCA) channels, epidermal growth factor receptor tyrosine kinase, and antiapoptotic factors (eg, Bcl-2). Identification of these targets is driving development of new pharmacotherapeutic compounds. Aside from specific instances in which a single mediator has a major impact on hypersecretion--for example, histamine in rhinitis--it is likely that compounds with broad-spectrum anti-inflammatory activity are more effective than compounds with restricted activity. However, certain highly specific targets, such as CLCA channels, seem to be intimately associated with development of a hypersecretory phenotype. Data from clinical trials with blockers of these targets are awaited with great interest, not only for disease management but also to determine the clinical benefit of selective inhibition of airway hypersecretion.
Rogers
Duncan F
DF
Thoracic Medicine, National Heart & Lung Institute, Imperial College, Dovehouse St, London SW3 6LY, UK. duncan.rogers@imperial.ac.uk
D001249:Asthma / Q000188:drug therapy / Q000378:metabolism*; D002199:Capillary Permeability; D018118:Chloride Channels / Q000037:antagonists & inhibitors; D005938:Glucocorticoids / Q000627:therapeutic use; D006633:Histamine Antagonists / Q000627:therapeutic use; D006801:Humans; D009093:Mucus / Q000378:metabolism*; D009297:Nasal Mucosa / Q000378:metabolism*; D012221:Rhinitis, Allergic, Perennial / Q000188:drug therapy / Q000378:metabolism*; D006255:Rhinitis, Allergic, Seasonal / Q000188:drug therapy / Q000378:metabolism*
D018118:Chloride Channels; D005938:Glucocorticoids; D006633:Histamine Antagonists