Mechanism of atp-induced leukocyte adherence to cultured pulmonary artery endothelial cells. Parker, Annie Lin, Laura L. Likar, Doloretta D. Dawicki, and Sharon Rounds. Pulmonary Medicine Section, Department of Medicine, Providence Veterans Affairs Medical Center and Brown University School of Medicine, Providence, Rhode Island
APStracts 2:0221L, 1995.
Previously we have shown that ATP enhances the adherence of HL- 60 cells and human neutrophils to bovine pulmonary artery endothelial cells. The current investigations extend earlier findings by showing that ATP and UTP dose-dependently stimulate human neutrophil adherence to human pulmonary artery endothelial cells. We have also explored the mechanisms of ATP and UTP stimulated adherence. We have found that fucose, a component of selectin receptors, inhibits ATP -stimulated HL-60 cell-bovine pulmonary artery endothelial cell adhesion. Additionally, pretreatment of HL-60 cells with neuraminidase abolishes ATP enhancement. However, fucose does not affect ATP, or thrombin, -induced adhesion of freshly isolated human neutrophils to human endothelial cells. Antibodies to human P -selectin, ICAM-1, and the [beta]-subunit of CD11/CD18 do not alter ATP-induced adherence of HL-60 cells to bovine endothelial cells. Similarly, antibodies to human P-selectin and ICAM-1 do not inhibit human neutrophil-human pulmonary artery endothelial cell adhesion. The platelet activating factor receptor antagonists, WEB 2086 and L -659,989, are effective in attenuating ATP and UTP stimulated adherence. Preincubation of neutrophils or human pulmonary artery endothelial cells with ATP or UTP also enhances adherence, an effect which is blocked by L659,989. Thus, platelet activating factor, associated with both neutrophils and endothelial cells, mediates ATP- and UTP-induced neutrophil adherence. ATP, released during vascular injury, may exacerbate neutrophil-endothelial cell interaction and thereby contribute to neutrophil induced injury. 

Received 23 November 1994; accepted in final form 30 November
1995.
APS Manuscript Number L339-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 12 December 95