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(American Journal of Pathology. 2000;157:1229-1237.)
© 2000 American Society for Investigative Pathology

Regular Articles

Induction of Vascular Adhesion Protein-1 during Liver Allograft Rejection and Concomitant Cytomegalovirus Infection in Rats

Timi Martelius^*, Marko Salmi, Hongyan Wu, Cathrien Bruggeman^§, Krister Höckerstedt^*, Sirpa Jalkanen and Irmeli Lautenschlager^*

From the Departments of Surgery^*
and Virology,
Helsinki University Hospital, and University of Helsinki, Helsinki, Finland: the MediCity Research Laboratory,
University of Turku, Turku, Finland; and the Department of Medical Microbiology,^§
University of Maastricht, Maastricht, The Netherlands

Vascular adhesion protein-1 (VAP-1) is an adhesion molecule controlling lymphocyte recirculation through high endothelial venules of the lymph nodes. It has also been shown to be induced and to mediate lymphocyte adhesion at sites of inflammation. We studied the expression of VAP-1 and two other inducible adhesion molecules ICAM-1 and VCAM-1 in our experimental model of rat liver allograft rejection and, in addition, the effect of concomitant rat cytomegalovirus (RCMV) infection on this expression. Expression of VAP-1, ICAM-1, and VCAM-1 was studied in rat liver allografts with or without RCMV infection, isografts, and normal rat liver. Immunoperoxidase technique and monoclonal antibodies including a novel anti-VAP-1 reagent were used. VAP-1 expression was induced by acute rejection in sinusoids, hepatocytes, and also in bile ducts, when compared to the isografts or normal liver, where only blood vessels were consistently positive. Sinusoidal and hepatocyte expression of VAP-1 was prolonged by the presence of RCMV. ICAM-1 and VCAM-1 expression was also induced by acute rejection. However, RCMV increased sinusoidal VCAM-1 expression compared to uninfected grafts. The present experimental study shows that VAP-1 is up-regulated in acute rejection of liver allografts, and that this up-regulation is prolonged by RCMV infection.

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