Functional alpha 1-protease inhibitor in the lower respiratory tract of cigarette smokers is not decreased

Cigarette smoking is the major risk factor for the development of pulmonary emphysema, a disorder that may result from an imbalance between the elastase and antielastase levels in the lungs. Decreased functional alpha 1-protease inhibitor, an inhibitor of neutrophil elastase, might render smokers su...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1983-09, Vol.221 (4616), p.1187-1189
Main Authors: Stone, P J, Calore, J D, McGowan, S E, Bernardo, J, Snider, G L, Franzblau, C
Format: Article
Language:English
Subjects:
Adult
Bronchi - metabolism
Female
Humans
In Vitro Techniques
Male
Neutrophils - metabolism
Protease Inhibitors - metabolism
Pulmonary Alveoli - metabolism
Smoking
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Summary:Cigarette smoking is the major risk factor for the development of pulmonary emphysema, a disorder that may result from an imbalance between the elastase and antielastase levels in the lungs. Decreased functional alpha 1-protease inhibitor, an inhibitor of neutrophil elastase, might render smokers susceptible to elastase-catalyzed destruction of pulmonary elastic fibers and the development of emphysema. Binding and inactivation of isotopically labeled porcine pancreatic elastase and human neutrophil elastase by alpha 1-protease inhibitor were measured in fluid obtained by bronchoalveolar lavage of volunteers. The inhibition of elastase-catalyzed solubilization of elastin and a tripeptide substrate were also determined. The mean level of functional alpha 1-protease inhibitor in the bronchoalveolar lavage fluid of smokers was found to be equal to or greater than that of nonsmokers, contradicting reports by other investigators. Increased elastase derived from pulmonary neutrophils, rather than decreased functional alpha 1-protease inhibitor, appears to be the main factor in the genesis of emphysema in smokers.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.6612333