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Neutrophil and monocyte adherence to and migration across monolayers of
cytokine-activated endothelial cells: the contribution of CD18, ELAM-1, and
VLA-4
BC Hakkert, TW Kuijpers, JF Leeuwenberg, JA van Mourik and D Roos
Central Laboratory of the Netherlands Red Cross Blood Transfusion Service,
Amsterdam.
Pretreatment of endothelial cells with cytokines enhances the adherence of
leukocytes, a process that is mediated by surface proteins expressed on
both cell types. A three-dimensional model system for the simultaneous
determination of leukocyte adherence and migration was used to study the
contribution of CD11/CD18, endothelial leukocyte- adhesion molecule-1
(ELAM-1) and VLA-4 in neutrophil and monocyte adherence to and migration
through cytokine-activated endothelial cells. Pretreatment of endothelial
cells for 4 hours with recombinant interleukin-1 beta (rIL-1 beta) was
found to enhance neutrophil adherence and migration to a much greater
extent than monocyte adherence and migration. Neutrophil adherence was
almost completely prevented by the combined use of monoclonal antibodies
(MoAbs) against ELAM-1 and CD18. Although ELAM-1 has been designated an
endothelial cell-specific cytokine-inducible receptor for neutrophils, we
observed that ENA2, an anti-ELAM-1 MoAb, significantly reduced monocyte
adherence about 30%. MoAbs against VLA-4, the ligand of the cytokine-
inducible receptor VCAM-1, did not affect monocyte adherence. However, the
combined use of the MoAbs against CD18, ELAM-1, and VLA-4 had a very strong
and additive inhibitory effect on rIL-1 beta-induced monocyte adherence.
The anti-CD18 MoAb reduced both rIL-1 beta-induced neutrophil and monocyte
migration far below the level of the unstimulated controls, whereas neither
the anti-ELAM-1 nor the anti-VLA- 4 MoAb significantly affected the process
of migration. Our results indicate that neutrophils and monocytes initially
adhere to cytokine- activated endothelial cells by CD18-independent and (to
a lesser extent) by CD18-dependent mechanisms and subsequently change gears
to a completely CD18-dependent migratory mechanism.
Volume 78,
Issue 10,
pp. 2721-2726,
11/15/1991
Copyright © 1991 by The American Society of Hematology
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