Da. Knight et al., Cytomegalovirus-mediated modulation of adhesion molecule expression by human arterial and microvascular endothelial cells, TRANSPLANT, 68(11), 1999, pp. 1814-1818
Background Cytomegalovirus (CMV), a betaherpes-virus associated with allogr
aft rejection, infects the endothelium, the cellular interface between allo
graft 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 ad
hesion molecule induction previously described on umbilical vein EC. Theref
ore, 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-alp
ha 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-alp
ha-mediated induction of these molecules.
Conclusion. CMV-induced modulations of adhesion molecule expression, which
may affect allograft immunogenicity, seem common to all EC regardless of va
scular origin.