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Blood, Vol. 94 No. 12 (December 15), 1999:
pp. 4020-4028
Platelet Factor 4-Induced Neutrophil-Endothelial Cell Interaction:
Involvement of Mechanisms and Functional Consequences Different
From Those Elicited by Interleukin-8
Frank Petersen,
Lothar Bock,
Hans-Dieter Flad, and
Ernst Brandt
From the Department of Immunology and Cell Biology, Research Center
Borstel, Borstel, Germany.
Platelet factor 4 (PF-4), a member of the CXC-subfamily of
chemokines, is secreted in high amounts by activated platelets. In
previous studies, we found that PF-4 specifically binds to human
polymorphonuclear granulocytes (PMN), but requires tumor necrosis
factor- (TNF-) as a costimulus for the induction of effector
functions in suspended cells. In the present study, we have examined
PF-4 in comparison with interleukin-8 (IL-8) for its ability to promote
interaction of PMN with cultured endothelial cells (EC). We show here
for the first time that PF-4 dose-dependently induces PMN to undergo
extremely firm adhesion to EC as well as to exocytose secondary granule
contents in the presence of these cells. Interestingly, costimulation
by TNF- was not required, indicating that EC could provide a
corresponding signal(s). As evident from antibody blocking experiments,
PF-4-induced adhesion involved PMN-expressed L-selectin as well as
leukocyte function-associated molecule-1 (LFA-1), whereas IL-8 involved
MAC-1. Because blocking antibodies to LFA-1 but not to
L-selectin or MAC-1 abrogated PF-4-dependent marker exocytosis from
PMN, the costimulatory signal provided by EC appears to be elicited
through cell-cell contact via LFA-1. IL-8, inducing the upregulation of
MAC-1, did not elicit marker exocytosis in contact with EC. Our results
suggest a role for PF-4 in the promotion of PMN-EC interaction that is
virtually different from that exhibited by other CXC-chemokines such as IL-8.
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