Ph-dependence of neutrophil-endothelial cell adhesion and adhesion molecule expression. Serrano, Carlos V., Jr., Aureliano Fraticelli, Rossella Paniccia, Anna Teti, Beth Noble, Stefano Corda, Tullio Faraggiana, Roy C. Ziegelstein, Jay L. Zweier, and Maurizio C. Capogrossi. Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224; Department of Medicine, Division of Cardiology, Johns Hopkins Bayview Medical Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224; Laboratorio di Cardiologia Sperimentale, INRCA, Ancona, Italy; Dipartimento di Medicina Sperimentale, Universit[grave]a dell'Aquila, Italy; Laboratorio di Patologia Vascolare, Istituto Dermopatico dell'Immacolata-IRCCS, Roma, Italy
APStracts 3:0066C, 1996.
Neutrophil adhesion to the vascular endothelium is enhanced during tissue ischemia/inflammation, conditions which are associated with tissue acidosis. This study examined the effects of hypercarbic acidosis (10% or 20% CO2) and of hypocarbic alkalosis (0% CO2) on human neutrophil CD18 and human aortic endothelial cell ICAM-1, VCAM -1 and E-selectin expression quantified by flow cytometry. Acidosis with 20% CO2 for 4 hours decreased ICAM-1 to 60.6+/-9.7% of control. In contrast, alkalosis with 0% CO2 for 4 hours enhanced ICAM-1 expression to 143.8+/-10.1 of control. There was no pH-dependence of VCAM-1 or E-selectin expression. Tumor necrosis factor-[alpha] (TNF -[alpha]; 10 ng/ml) increased endothelial ICAM-1, E-selectin, and VCAM-1; under these conditions, acidosis with 20% CO2 blunted both ICAM-1 and E-selectin surface expression compared to 5% CO2-, TNF -[alpha]-treated cells. Hypercarbic acidosis with 20% CO2 increased neutrophil CD18 expression and enhanced neutrophil adhesion. This latter effect was inhibited by neutrophil pretreatment with an anti -CD18 monoclonal antibody. In contrast, when only endothelial cells were pre-incubated with the hypercarbic buffer, neutrophil adhesion diminished to 55.6+/-7.8% of control. The results suggest that acidosis generated during tissue ischemia/inflammation may induce CD18-mediated neutrophil adhesion despite a decrease in ICAM-1 expression. 

Received 2 March 1995; accepted in final form 22 February 1996.
APS Manuscript Number C120-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 March 96