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1
British Heart Foundation Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom
We have studied vascular endothelial activation and increased
expression of ICAM-1 and VCAM-1 at the onset of the elicitation phase
of oxazolone contact hypersensitivity in mice. By measuring the local
uptake of i.v. administered radiolabeled anti-ICAM-1 and
anti-VCAM-1 mAb, we found that endothelial ICAM-1 and VCAM-1 was
increased by 4 h after challenge, 2 h later than the first
peak of ear swelling and 125I-labeled human serum albumen
uptake. Increased expression of endothelial ICAM-1 and VCAM-1 was
significantly greater in sensitized animals than in naive animals.
Anti-TNF-
antiserum significantly inhibited both the increase in ear
thickness (p < 0.01), and the up-regulation of
ICAM-1 and VCAM-1 expression (p < 0.01 for both)
at 4 h. In contrast, the combination of anti-IL-1 and
IL-1ß had only a small inhibitory effect on ICAM-1 expression
(p < 0.05) and no significant effect on increased
ear thickness or on VCAM-1 expression. A mixture of anti-TNF-,
anti-IL-1, and IL-1ß was no more inhibitory for endothelial
ICAM-1 and VCAM-1 expression than anti-TNF- alone. ICAM-1 and
VCAM-1 expression at 4 h was unaffected by a combination of mAb
against 4 and ß2 integrins, whereas
expression at 24 h was significantly inhibited
(p < 0.05), suggesting that the release of TNF-
and other cytokines involved in the initiation of the response may not
require leukocyte traffic or other leukocyte functions involving these
integrins. We conclude that the early up-regulation of endothelial
ICAM-1 and VCAM-1 during the elicitation of contact hypersensitivity is
primarily due to the immune-dependent local release of
TNF-.
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