title: Aortic endothelium in HIV-1 infection: chronic injury, activation, and increased leukocyte adherence.
abstract: Clinical and serological studies provide evidence for a pathogenetically relevant vasculopathy in acquired immune deficiency syndrome (AIDS); however, the morphological status of the endothelium under conditions of human immunodeficiency virus (HIV)-1 infection is only sparsely documented. In this study we adapted an en face preparation technique of endothelium for use in immunohistochemistry and investigated the aortic endothelium of pre-AIDS and AIDS patients (n = 32) in comparison with an HIV-negative group (n = 17). The control group showed a regular pattern of evenly distributed aortic endothelial cells, whereas the endothelial cell pattern in the HIV-1-infected patients was clearly disturbed. Simultaneously, the degree of leukocyte adherence on the aortic endothelium increased significantly. These changes were accompanied by an up-regulation of the vascular cell adhesion molecule-1 (VCAM-1) and E-selectin (ELAM-1). The endothelium turnover increased, and one-half of the HIV-1-infected patients exhibited HLA-DR (major histocompatibility complex class II) antigen in the aortic endothelium. Our results provide evidence for a profound and repeated injury with regeneration and activation of the endothelium in HIV-1 infection. Injury as well as activation of the endothelium impairs its normal regulatory properties. This could have consequences for the maintenance of the blood-brain barrier; it might influence the immunologically important interaction of the endothelium with T cells; and it might trigger Kaposi's sarcoma.
authors.affiliation: Department of Pathology, Ludwig Maximilians University of Munich, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Zietz
authors.forename: B
authors.initials: B
authors.lastname: Hotz
authors.forename: M
authors.initials: M
authors.lastname: Stürzl
authors.forename: E
authors.initials: E
authors.lastname: Rauch
authors.forename: R
authors.initials: R
authors.lastname: Penning
authors.forename: U
authors.initials: U
authors.lastname: Löhrs
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000473:pathology*; D000293:Adolescent; D000328:Adult; D000911:Antibodies, Monoclonal / Q000276:immunology; D001011:Aorta / Q000473:pathology / Q000821:virology; D001012:Aorta, Abdominal / Q000473:pathology / Q000821:virology; D001018:Aortic Diseases / Q000473:pathology* / Q000821:virology; D002448:Cell Adhesion; D002455:Cell Division; D002648:Child; D019040:E-Selectin / Q000096:biosynthesis; D004730:Endothelium, Vascular / Q000473:pathology* / Q000821:virology; D005260:Female; D015497:HIV-1 / Q000254:growth & development*; D006684:HLA-DR Antigens / Q000096:biosynthesis; D006801:Humans; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D007375:Interleukin-1 / Q000096:biosynthesis; D019394:Ki-67 Antigen / Q000032:analysis; D007962:Leukocytes / Q000473:pathology* / Q000821:virology; D008297:Male; D008875:Middle Aged; D014775:Virus Activation
chemical_list: D000911:Antibodies, Monoclonal; D019040:E-Selectin; D006684:HLA-DR Antigens; D007375:Interleukin-1; D019394:Ki-67 Antigen; D018799:Intercellular Adhesion Molecule-1