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Intercellular adhesion molecule-1 mediates the expression of monocyte-
derived MIP-1 alpha during monocyte-endothelial cell interactions
NW Lukacs, RM Strieter, VM Elner, HL Evanoff, M Burdick and SL Kunkel
Department of Pathology, University of Michigan Medical School, Ann Arbor
48109-0602.
The extravasation of leukocytes from the lumen of the vessel to a site of
inflammation initially requires a specific binding event followed by
migration of the cells through the endothelial cell layer into the
inflammatory foci. The interaction of leukocytes with the endothelium via
specific receptors may provide intracellular signals that activate the
cells. In the present study we have investigated the production of MIP-1
alpha, a mononuclear cell chemotactic protein, during monocyte:endothelial
cell interactions. Neither unstimulated nor interferon (IFN)-stimulated
human umbilical vein endothelial cells (HUVECs) produced substantial MIP-1
alpha protein. However, the addition of enriched monocyte populations with
unstimulated HUVECs resulted in the production of MIP-1 alpha. Monocytes
cultured with IFN- gamma-activated HUVECs showed an additional increase in
MIP-1 alpha production. Immunohistochemical analysis demonstrated that the
monocyte was the cellular source of MIP-1 alpha production in this
coculture system. The mechanism of MIP-1 alpha expression was further
assessed by determining the role of adhesion molecules in the regulation of
MIP-1 alpha production during monocyte:HUVEC interactions. To attenuate the
increased production of MIP-1 alpha by the monocyte:HUVEC interaction,
anti-adhesion molecule monoclonal antibodies (MoAbs) were added to the
cultures. Addition of anti-ICAM-1 neutralizing MoAbs significantly
inhibited the production of MIP-1 alpha, whereas neutralizing anti-VCAM- 1
MoAbs failed to block MIP-1 alpha production. Furthermore, MIP-1 alpha
production was induced in monocytes cultured on ICAM-1-coated plates. These
results indicate an intimate relationship between leukocyte-endothelial
cells, adhesion molecule, and the expression of the monocyte-derived
chemokine MIP-1 alpha during cellular adhesion. This mechanism may serve an
important role in cell activation and recruitment of leukocytes during the
initiation of an inflammatory response.
Volume 83,
Issue 5,
pp. 1174-1178,
03/01/1994
Copyright © 1994 by The American Society of Hematology
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