Human alveolar macrophage proteolytic enzyme activities in chronic obstructive pulmonary disease. Lack of correlation with functional abnormalities.
The occurrence of emphysema in people deficient in alpha1-antitrypsin and the production of emphysema in experimental animals with elastolytic enzymes suggest proteolysis as a mechanism for the development of emphysema. To investigate the possible role of pulmonary alveolar macrophages in the pathogenesis of emphysema, we measured elastase, acid protease, and elastase-like esterase activities in macrophages from patients with chronic obstructive lung disease and attempted to correlate the level of enzyme activity with the severity of pulmonary function abnormality measured in these patients. Compared to values for cigarette smokers with normal pulmonary function, these macrophage enzyme activities were not increased in patients with chronic obstructive lung disease, and there was no correlation of high elastase activity with more severe degrees of pulmonary function abnormality. These findings lead us to believe that the absolute level of proteolytic enzymes in pulmonary alveolar macrophages is not in itself a determinant of emphysema.
D000328:Adult; D000368:Aged; D002283:Carcinoma, Bronchogenic / Q000201:enzymology; D004950:Esterases / Q000378:metabolism; D005260:Female; D006801:Humans; D008173:Lung Diseases, Obstructive / Q000201:enzymology*; D008175:Lung Neoplasms / Q000201:enzymology; D008264:Macrophages / Q000201:enzymology*; D008297:Male; D008875:Middle Aged; D010196:Pancreatic Elastase / Q000378:metabolism; D010447:Peptide Hydrolases / Q000378:metabolism*; D011650:Pulmonary Alveoli / Q000201:enzymology*; D011656:Pulmonary Emphysema / Q000201:enzymology; D012907:Smoking / Q000503:physiopathology
D004950:Esterases; D010447:Peptide Hydrolases; D010196:Pancreatic Elastase