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Section of Allergy and Clinical Immunology, Department of Medicine, University of Wisconsin, Madison, WI 53792
In bronchial asthma, eosinophils (EOS) adhere to, and migrate
across, the lung microvasculature to exert their effector functions in
the airways. This study was conducted to determine the effect of
cytokines on adhesion molecule expression on human pulmonary
microvascular endothelial cells (HPMEC) and the influence of these
molecules on EOS adhesion and transmigration in vitro. Unlike ICAM-1
expression (>80% positive cytokine-treated HPMEC by flow cytometry),
VCAM-1 expression varied with the cytokine(s) pretreatment; the order
of potency was: TNF-
+ IL-4 (82.2 ± 4.2% positive cells) >
TNF- (41.8 ± 5.1%) > IL-1ß (20.8 ± 4.7%). IL-4
alone had no effect on either ICAM-1 or VCAM-1 expression. EOS adhesion
to cytokine-treated HPMEC followed the same order as that observed for
VCAM-1 expression. Interestingly, EOS migration across cytokine-treated
HPMEC varied inversely with VCAM-1 expression on, and EOS adhesion to,
HPMEC; IL-1ß (21.2 ± 1.4% migration) > TNF- (12.6 ±
2.6%) > TNF- + IL-4 (9.1 ± 2.0%). EOS adhesion was greatest
with TNF- + IL-4-treated HPMEC, was dependent on VCAM-1, and
inhibited with anti-4 integrin mAb (67.7
± 7.5% inhibition, p < 0.0005). In contrast, the
highest EOS migration occurred across IL-1ß-treated HPMEC and was
inhibited by anti-ß2 integrin mAb (40.4 ± 2.5%
inhibition, p < 0.005). Viable HPMEC were required
for EOS migration but not adhesion. Our results suggest that EOS
adhesion and transmigration are differentially regulated by VCAM-1 and
ICAM-1 expression and the interaction of these adhesion proteins with
their respective counterligands, i.e., 4 and
ß2 integrins on EOS.
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