title: Induction of vascular adhesion protein-1 during liver allograft rejection and concomitant cytomegalovirus infection in rats.
abstract: 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.
authors.affiliation: Departments of Surgery and Virology, Helsinki University Hospital, and University of Helsinki, Helsinki, Finland. tmarteli@helsinki.fi
authors.forename: T
authors.initials: T
authors.lastname: Martelius
authors.forename: M
authors.initials: M
authors.lastname: Salmi
authors.forename: H
authors.initials: H
authors.lastname: Wu
authors.forename: C
authors.initials: C
authors.lastname: Bruggeman
authors.forename: K
authors.initials: K
authors.lastname: Höckerstedt
authors.forename: S
authors.initials: S
authors.lastname: Jalkanen
authors.forename: I
authors.initials: I
authors.lastname: Lautenschlager
mesh_terms: D000208:Acute Disease; D006631:Amine Oxidase (Copper-Containing) / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D016466:CHO Cells; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism*; D006224:Cricetinae; D003586:Cytomegalovirus Infections / Q000150:complications* / Q000378:metabolism*; D006084:Graft Rejection / Q000150:complications* / Q000378:metabolism*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D016031:Liver Transplantation; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011914:Rats, Inbred BN; D011919:Rats, Inbred Strains; D012016:Reference Values; D013997:Time Factors; D014184:Transplantation, Homologous; D014185:Transplantation, Isogeneic; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D015815:Cell Adhesion Molecules; D012333:RNA, Messenger; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; C076668:AOC3 protein, human; D006631:Amine Oxidase (Copper-Containing)