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Mechanisms of Airway Hypersecretion and Novel Therapy*

Jay A. Nadel, MD
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*From the Cardiovascular Research Institute, and Departments of Medicine and Physiology, University of California San Francisco, San Francisco, CA.

Correspondence to: Jay A. Nadel, MD, Division of Pulmonary and Critical Care Medicine, University of California San Francisco, CVRI, 505 Parnassus Ave, M-1325, San Francisco, CA 94143-0130; e-mail: janadel@itsa.ucsf.edu



Chest. 2000;117(5_suppl_1):262S-266S. doi:10.1378/chest.117.5_suppl_1.262S-a
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Abbreviations: AB = alcian blue; EGF = epidermal growth factor; IP = intraperitoneal; IT = intratracheal; OVA = ovalbumin; PAS = periodic acid-Schiff; TGF = transforming growth factor; TNF = tumor necrosis factor

Hypersecretion is an important feature in many chronic airway diseases, including COPD,1 cystic fibrosis,2 bronchiectasis,3 and acute asthma.4 Mucus secretion is derived from airway submucosal glands and from goblet cells lining the airway epithelium. Submucosal glands are located in large conducting airways, where their ducts empty onto the airway luminal surface, preferentially at airway bifurcations adjacent to cough receptor endings. Therefore, it is not surprising that gland hypersecretion is associated with cough. Early investigators showed that airway obstruction in COPD originates in the periphery, and they showed that this obstruction is related to mortality. In 1989, Speizer et al5 concluded that a simple measure of lung function (FEV1) is an important predictor of COPD mortality. Cough and sputum production showed no (or only a weak) correlation with mortality. Subsequently, many investigators provided evidence that phlegm was of no predictive value when controlling for level of ventilatory impairment and smoking.,57 From these findings, one may conclude that airway hypersecretion from hyperplastic glands may cause distressing symptoms, but is not likely to be a major cause of death COPD.

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