Many of the features of bronchial disease are believed to be caused by dama
ge to the airways by elastase released by recruited neutrophils. There have
been few studies of the mechanisms involved and the interrelationships bet
ween components of the inflammatory process. We studied secretions from pat
ients with chronic bronchitis in the stable state. We assessed the presence
of neutrophils by measuring myeloperoxidase (MPO) activity and active neut
rophil elastase (NE). These results were compared with the chemoattractants
interleukin-8 (IL-8) and leukotriene B-4 (LTB4), the bronchial inhibitor s
ecretory leukoprotease inhibitor (SLPI), and protein leak (sputum/serum alb
umin ratio). MPO correlated with NE activity (r = 0.68, p < 0.001) and both
IL-8 (r = 0.52, p < 0.001) and LTB4 (r = 0.41, p < 0.001) indicating an as
sociation with the chemoattractants. Elastase activity correlated with IL-8
(r = 0.55, p < 0.001) and LTB4 (r = 0.41, p < 0.001) but negatively with S
LPI (r = -0.49, p < 0.001). NE also correlated positively with protein leak
(r = 0.36, p < 0.001), suggesting a cause and effect. MPO and protein leak
correlated negatively with FEV1 (percentage of predicted) only in patients
with chronic obstructive pulmonary disease (COPD) without alpha(1)-antitry
psin deficiency (r = -0.37, p < 0.001; r = -0.42, p < 0.01, respectively).
These complex interactions provide a template for future studies with speci
fic inhibitors or agonists which will clarify the role of individual factor
s.