The Elastase Inhibitory Capacity and the α1-Proteinase Inhibitor and Bronchial Inhibitor Content of Bronchoalveolar Lavage Fluids from Healthy Subjects

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Abstract
Pulmonary emphysema is currently thought to be due to an elastase-antielastase imbalance with resultant destruction of alveolar structures. The present study was aimed at testing whether .alpha.1-proteinase inhibitor (.alpha.1PI) is the major component of the antielastase screen of the lower respiratory tract of healthy subjects. Bronchoalveolar lavage was performed in 8 nonsmokers (27.8 .+-. 0.96 years). The lavage fluids were tested for leukocyte and pancreatic elastase inhibitory capacity (LEIC and PEIC) and immunoreactive .alpha.1PI and bronchial inhibitor (brI) content. The mean .+-. s.e.m. levels of LEIC, PEIC, .alpha.1PI and brI were 0.16 .+-. 0.039, 0.042 .+-. 0.006, 0.09 .+-. 0.007 and 0.013 .+-. 0.002 mol/mol albumin, respectively. Thus, on the average, the molar concentration of brI was about 14% that of .alpha.1PI. The difference between LEIC and .alpha.1Pi did not reach statistical significance (P = 0.0503). The PEIC was however significantly lower than the .alpha.1 PI levels (P < 0.05), indicating that the lavage fluids contained both active and inactive .alpha.1PI. Nonsmokers and smokers did not differ in their LEIC, PEIC, .alpha.1PI and brI levels. When the data were examined on an individual basis, the subjects could be divided into 2 groups: group I (n = 9; 3 nonsmokers, 6 smokers) whose LEIC/.alpha.1PI molar ratios were higher than unity and group II (n = 8; 5 nonsmokers, 3 smokers) whose LEIC/.alpha.1PI molar ratios were equal or lower than unity. Group I subjects had significantly higher LEIC values (0.26 .+-. 0.05 mol elastase inhibited/mol albumin) than group II individuals (0.055 .+-. 0.006; P < 0.001) but the two groups had similar levels of immunoreactive .alpha.1PI (0.09 and 0.08 mol .alpha.1PI/mol albumin for group I and II, respectively), functionally active .alpha.1PI (percentage of active .alpha.1PI: 53% and 37% for group I and II, respectivel) and immunoreactive brI (0.016 and 0.010 mol brI/mol albumin for group I and II, respectively). These results suggested that the lavage fluids from group I contained significant amounts of undefined leukocyte elastase inhibitor(s). Gel filtration of a lavage fluid from group I showed that the undefined elastase inhibitor(s) co-eluted with brI. Most of the lavage fluids were still able to inhibit leukocyte elastase following removal of .alpha.1PI by perchloric acid precipitation. The mean LEIC of the acid-treated fluids (15.4 .+-. 2.7 .times. 10-8 M), was significantly higher than their mean brI concentration (2.3 .+-. 0.6 .times. 10-8 M); (P < 0.01), confirming the occurrence of undefined elastase inhibitors. The LeIC/brI molar ratios were greater than 1 in 13.17 acid-treated fluids. The highest ratios were found in group I subjects, confirming that the antielastase screen of these subjects is mainly composed of elastase inhibitors different from .alpha.1PI and brI. Removal of brI from some acid-treated fluids by immunoadsorption did not abolish the LEIC of these fluids.

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