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* From the Cardiovascular Research Institute, Departments of Medicine and Physiology, University of California, San Francisco, CA.
Correspondence to: Jay A. Nadel, MD, University of California, San Francisco, CVRI, 505 Parnassus Ave, M-1325, San Francisco, CA 94143-0130; e-mail: janadel{at}itsa.ucsf.edu
A common feature of COPD and other chronic lung diseases is hypersecretion of mucus into the airways, causing peripheral airway plugging and further airflow obstruction. The mucus is secreted by goblet cells, which are present in excessive numbers in COPD. This review describes how neutrophils in the airways of COPD patients stimulate the goblet cells to secrete their products. Recent findings on the mechanisms of neutrophil stimulation of goblet cell degranulation are discussed. These implicate the proteolytic enzyme elastase and cell surface adhesion molecules, and provide a basis for the investigation of potential novel therapies.
Key Words: CD11b/CD18 • hypersecretion • goblet cell degranulation • intercellular adhesion molecule-1 • neutrophil elastase
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