Addition of cultured and then carefully-washed bovine pulmonary artery
endothelial cells (EC) decreased (p < 0.05) human neutrophil elastase
activity (HNE) in vitro. HNE activity was also decreased (p < 0.05) b
y addition of histone or protamine treated EC. However, addition of pa
pain or trypsin treated EC decreased HNE activity less than addition o
f untreated cells suggesting that a protein rather than a difference i
n cell surface charge was responsible. Other observations suggest that
EC anti-elastolytic activity was not due to binding of antiprotease f
rom culture media but was dependent on EC protein synthesis. First, ad
dition of EC grown previously in serum-free media decreased HNE activi
ty the same (p < 0.05) as addition of EC cultured in media containing
serum. Second, addition of EC treated beforehand with cycloheximide de
creased HNE activity less than (p < 0.05) addition of untreated contro
l EC. We conclude that EC most likely make and have antielastolytic ac
tivity on their surfaces and speculate that EC associated anti-elastol
ytic activity may modulate inflammatory, repair and other biologic pro
cesses involving neutrophil elastase.