The effect of herpesvirus infection on the expression of cell adhesion molecules on cultured human dermal microvascular endothelial cells.

Cell-mediated immune response to herpes simplex virus (HSV) may be important in the pathogenesis of herpes keratitis, erythema multiforme or Behcet's disease. We examined whether herpesvirus infection regulates the expression of cell adhesion molecules on cultured human dermal microvascular endothelial cells (HDMEC) and the regulation of T-lymphocytes binding to HDMEC. The expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), or E-selectin on HDMEC increased significantly after treatment with HSV-1, HSV-2, or measles virus on HDMEC. Anti-IL-1 alpha antibody or anti-TNF alpha antibody partially inhibited the expression of ICAM-1, VCAM-1, or E-selectin on HDMEC. The binding of T-lymphocytes to HDMEC increased significantly after the treatment of HSV-1 or measles virus on HDMEC. The binding of T-lymphocytes to HDMEC was significantly inhibited after 16 h of incubation following treatment with anti-ICAM-1 antibody, anti-IL-1 alpha antibody or anti-TNF alpha antibody to HDMEC. These study results suggest that HSV induces the increased expression of ICAM-1, or induction of VCAM-1 and E-selectin on HDMEC and that among these adhesion molecules, the expression of ICAM-1 on HDMEC mainly regulates the binding of T-lymphocytes to HDMEC. The data also suggest that IL-1 alpha or TNF alpha which was produced by HSV infected HDMEC may be related to these events.