Cytomegalovirus-mediated modulation of adhesion molecule expression by human arterial and microvascular endothelial cells.
BACKGROUND
Cytomegalovirus (CMV), a betaherpesvirus associated with allograft rejection, infects the endothelium, the cellular interface between allograft tissue and the host immune system. Because of recent appreciation of the phenotypic diversity of endothelial cells (EC) from different vascular compartments, controversy now exists on the universality of CMV-mediated adhesion molecule induction previously described on umbilical vein EC. Therefore, we herein extend these previous studies to arterial and microvascular EC, which represent sites of vascular rejection.


METHODS
Human coronary artery, aortic, umbilical artery, and microvascular EC were mock or CMV infected and/or treated with tumor necrosis factor-a before flow cytometric and immunohistochemical analysis.


RESULTS
CMV directly enhanced intercellular adhesion molecule-1 on all EC isolates but did not induce E-selectin or vascular cell adhesion molecule-1. Furthermore, CMV-infected EC were refractory to tumor necrosis factor-alpha-mediated induction of these molecules.


CONCLUSIONS
CMV-induced modulations of adhesion molecule expression, which may affect allograft immunogenicity, seem common to all EC regardless of vascular origin.
Knight
D A
DA
Department of Pathology, Ohio State University College of Medicine and Public Health, Columbus 43210-1218, USA.
Waldman
W J
WJ
Sedmak
D D
DD
D001158:Arteries / Q000378:metabolism*; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D003586:Cytomegalovirus Infections / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism*; D005434:Flow Cytometry; D006801:Humans; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008833:Microcirculation; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D015815:Cell Adhesion Molecules; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1