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A Juxtacrine Mechanism for Neutrophil Adhesion on Platelets Involves
Platelet-Activating Factor and a Selectin-Dependent Activation Process
Lena Ostrovsky,
Alison J. King,
Samantha Bond,
Debra Mitchell,
Diane E. Lorant,
Guy A. Zimmerman,
Robert Larsen,
Xiao Fe Niu, and
Paul Kubes
From the Department of Medical Physiology and Medicine, University of
Calgary, Calgary, Alberta, Canada; the Nora Eccles Harrison
Cardiovascular Research and Training Institute, and Department of
Internal Medicine, University of Utah School of Medicine, Salt Lake
City, UT; and Glycomed Inc, Ameda, CA.
The aim of this study was to identify the molecular mechanisms
involved in neutrophil adhesion to immobilized platelets with particular focus on the possible existence of a juxtacrine system for
neutrophil-platelet interactions. Platelets were immobilized onto
collagen (type I)-coated coverslips that were placed in a flow chamber
and neutrophils were perfused across these confluent monolayers at a
shear stress of 1 to 4 dynes/cm2. Neutrophils rolled, and a
significant proportion (25% to 50%) adhered to platelet monolayers.
P-selectin was expressed in very large quantities on the surface of
platelets and mediated all of the rolling, whereas the
 2-integrin mediated firm adhesion. An activation
mechanism for adhesion was necessary inasmuch as fixed neutrophils
continued to roll on immobilized platelets, but did not adhere.
Platelets adherent to collagen produced significant levels of
platelet-activating factor (PAF). Accordingly, the firm adhesion of
neutrophils to platelets was significantly inhibited by a PAF receptor
antagonist (WEB 2086). Treatment of only the platelets with
acetylhydrolase, which converts membrane-associated PAF to lyso-PAF,
prevented 60% of the adhesion. These data suggest that PAF, on the
surface of platelets, mediated a significant portion of the adhesive
interaction. Addition of some selectin-binding carbohydrates (fucoidan
or soluble SLEx analogs but not dextran sulfate) to the
platelets caused rolling neutrophils to immediately adhere, an event
that was not observed on histamine or thrombin-treated endothelium or
P-selectin transfectants. These data support the view that a juxtacrine
activation process exists on immobilized platelets for neutrophils.
This process can be greatly enhanced on platelets and may involve a
signaling mechanism through P-selectin.
Blood, Vol. 91 No. 8 (April 15), 1998:
pp. 3028-3036
© 1998 by The American Society of Hematology.
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