Am. J. Respir. Crit. Care Med., Vol 152, No. 5, Nov 1995, 1592-1598.
Contribution of secretory leukocyte proteinase inhibitor to the antiprotease defense system of the peripheral lung: effect of ozone- induced acute inflammation
C Nadziejko, I Finkelstein and JR Balmes
Institute of Environmental Medicine, New York University Medical Center, Tuxedo 10987, USA.
Secretory leukocyte protease inhibitor (SLPI) and elafin are structurally
similar, low-molecular-weight antiproteases produced in the lung. We have
developed a simple method for distinguishing the antiprotease activities of
SLPI and elafin in lung lavage fluid from those of alpha 1-antitrypsin
(alpha 1-AT) that is based on the resistance of the low-molecular-weight
antiproteases to inactivation by cetyltrimethylammonium bromide. In a study
of 23 healthy, nonsmoking volunteers, we found that the
low-molecular-weight antiproteases accounted for 22 +/- 2% (mean +/- SEM, n
= 23) of the total neutrophil elastase-inhibitory capacity of human
bronchoalveolar lavage fluid (BALF). Elafin activity was below the limit of
detection. SLPI activity (as measured by inhibition of alpha-chymotrypsin)
accounted for 72 +/- 4% (mean +/- SEM, n = 23) of the low-molecular-weight
antiprotease activity in BALF. Measurements of SLPI in the lavage fluid
samples by enzyme-linked immunosorbent assay (ELISA) agreed closely with
values obtained by measuring the activity of this inhibitor. The activity
of the low-molecular-weight antiproteases decreased significantly (p <
0.05), from 9.0 +/- 0.8 to 7.0 +/- 0.6 pmol of neutrophil elastase
inhibited per mL (mean +/- SEM, n = 23), following acute ozone exposure.
