During inflammation leukocytes are playing a tremendous role in the de
fense against bacterial infections. Tumor necrosis factor alpha (TNF a
lpha) increases adhesion of leukocytes to endothelial cells. The non s
teroidal anti-inflammatory drug ibuprofen is able to reduce inflammato
ry processes in humans and is a widely used drug. The influence of ibu
profen on TNF-alpha-induced expression of adhesion molecules on endoth
elial cells is well investigated and has been published recently by ou
r group. For leukocyte migration, leukocytes have to attach and finall
y migrate through monolayers of endothelial cells. The aim of the curr
ent study was to investigate leukocyte migration through endothelial c
ell monolayers (ECM) under ibuprofen using a migration assay system. I
buprofen was identified as a potent inhibitor of the leukocyte migrati
on through endothelial cell monolayers in a dose dependent manner. The
treatment of either leukocytes (87 +/- 17.6 %; p>0.05) or endothelial
cell monolayers (62.5 +/- 9.4 %; p<0.05) showed that the influence is
more mediated through endothelial cells, the treatment of both cell t
ypes demonstrated an additive effect. In conclusion, the previously pu
blished changes of adhesion molecules on endothelial cells could be co
nfirmed with this functional migration test. The inhibition of the leu
kocyte migration may contribute to the anti-inflammatory actions of th
e drug.