Modulation of HLA class I antigen and ICAM‐2 on endothelial cells after in vitro infection with human cytomegalovirus

Abstract

Summary The aim of the present work is to investigate the expression of HLA class I antigen and intercellular adhesion molecule-2 (ICAM-2) on the surface of human umbilical cord endothelial cells (HUVEC) after infection with human cytomegalovirus (HCMV). The expression of HLA class I antigen and ICAM-2 were determined (using antibodies against HLA class I antigen and ICAM-2) by attachment inhibition assay and¯ow cytometric analysis. Attachment inhibition assay demonstrated that HCMV increased the expression of HLA class I antigen. This was con®rmed by¯ow cytometric analysis, which showed an increase in HLA class I antigen expression on HCMV-infected HUVEC. The results of the expression of ICAM-2 using attachment inhibition assay revealed that ICAM-2 is involved signi®cantly in the increased adhesion of T lymphocytes to HCMV-infected HUVEC. However,¯ow cytometric analysis revealed that there were no changes in the expression of ICAM-2 on HCMVinfected HUVEC. One possible explanation for this is that HCMV induces the activation of ICAM-2 on the surface of HCMV-infected endothelial cells without a ecting its expression.

Human Cytomegalovirus Induces a Biphasic Inflammatory Response in Primary Endothelial Cells

“…Studies report that hCMV induces production of the EC proinflammatory mediators interleukin 8 (IL-8) (4,5) and IL-6 (6) and expression of the leukocyte adhesion receptor ICAM-1 (7,8). In addition, reports have shown that hCMV-infected EC (hCMV-EC) supported enhanced leukocyte recruitment (5,(9)(10)(11). These heavily cited studies, particularly those demonstrating a role for hCMV-induced IL-8 in neutrophil transmigration (4,5), support the idea that hCMV contributes to the development or exacerbation of inflammatory pathologies.…”