Publication Date:
1983-09-16
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, P J -- Calore, J D -- McGowan, S E -- Bernardo, J -- Snider, G L -- Franzblau, C -- HL-19717/HL/NHLBI NIH HHS/ -- HL-25229/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 16;221(4616):1187-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612333" target="_blank"〉PubMed〈/a〉
Keywords:
Adult
;
Bronchi/*metabolism
;
Female
;
Humans
;
In Vitro Techniques
;
Male
;
Neutrophils/metabolism
;
Protease Inhibitors/*metabolism
;
Pulmonary Alveoli/*metabolism
;
*Smoking
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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