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Research Article Free access | 10.1172/JCI109811
Infectious Diseases Section and Connective Tissue Research Institute, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104
School of Medicine, Philadelphia, Pennsylvania 19104
University City Science Center, Philadelphia, Pennsylvania 19104
Find articles by MacGregor, R. in: JCI | PubMed | Google Scholar
Infectious Diseases Section and Connective Tissue Research Institute, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104
School of Medicine, Philadelphia, Pennsylvania 19104
University City Science Center, Philadelphia, Pennsylvania 19104
Find articles by Friedman, H. in: JCI | PubMed | Google Scholar
Infectious Diseases Section and Connective Tissue Research Institute, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104
School of Medicine, Philadelphia, Pennsylvania 19104
University City Science Center, Philadelphia, Pennsylvania 19104
Find articles by Macarak, E. in: JCI | PubMed | Google Scholar
Infectious Diseases Section and Connective Tissue Research Institute, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104
School of Medicine, Philadelphia, Pennsylvania 19104
University City Science Center, Philadelphia, Pennsylvania 19104
Find articles by Kefalides, N. in: JCI | PubMed | Google Scholar
Published June 1, 1980 - More info
Adherence of human granulocytes was measured on endothelial monolayers of human and bovine origin, grown in 35-mm Diam petri dishes and in cluster wells. Adherence to human endothelium in petri dishes using 1.0 ml of whole blood averaged 17.9±3.7%, and to bovine endothelium was 20.3±3.7%. Cluster wells required only 1/5 the endothelial cells needed for petri dishes, and 0.25 ml of whole blood yielded average adherence of 26.2±3.4 to human cells and 28.0±3.7 to bovine in the wells. The impact of infection of the endothelium by different viruses on subsequent granulocyte adherence was measured. Polio virus produced an acute lytic infection of human endothelial cells, with associated increased adherence to 185.4% of control 24 h after inoculation. Significantly increased adherence was noted at 6 h, before detectable cytopathic effect. Herpes simplex type I caused a similar rapidly lytic infection of bovine endothelium associated with increased adherence to 213.7% of control 6 h after inoculation. This augmented adherence could be demonstrated when granulocytes were suspended in physiologic saline solution, showing that antibody and complement need not be present. Trypsin treatment of infected monolayers did not prevent the augmentation, and supernate from infected monolayers increased the adherence of polymorphonuclear leukocytes to normal, uninfected monolayers. Chronic, slowly lytic infections, lasting 7 d or more, were induced with adenovirus in human endothelium and with measles virus in bovine cells. Adherence increased as virus was noted in the cell cultures on day 4, several days before cytotoxicity was seen. Thus, chronic viral infection of the endothelium appears possible, and results in increased granulocyte adherence. In naturally occurring disease, such an infection may act synergistically with adherent granulocytes to damage the endothelium, and may represent an in vitro model of vasculitis.
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