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Alterations in the Expression of ELAM‐1, ICAM‐1 and VCAM‐1 after In Vitro Infection of Endothelial Cells with a Clinical Isolate of Human Cytomegalovirus
Author(s) -
Shahgasempour Shapour,
Woodroffe Salwa B.,
Garnett Helen M.
Publication year - 1997
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1997.tb01177.x
Subject(s) - vcam 1 , human cytomegalovirus , biology , downregulation and upregulation , icam 1 , cell adhesion molecule , in vitro , flow cytometry , cell adhesion , endothelial stem cell , intercellular adhesion molecule 1 , adhesion , immunology , virology , microbiology and biotechnology , cell , virus , chemistry , biochemistry , organic chemistry , gene
Human cytomegalovirus (HCMV) infection of endothelial cells resulted in increased adhesion of the cells to peripheral blood leukocytes. It was demonstrated by flow cytometry that increased adhesiveness parallels the increased expression of cell surface adhesion molecules (ELAM‐1, ICAM‐1, VCAM‐1). The increased adhesion of PMN and T‐lymphocytes was due to upregulation in the expression of ELAM‐1 and ICAM‐1. The upregulation of VCAM‐1 resulted in the increased adhesiveness of monocytes and T‐lymphocytes to HCMV‐infected HUVEC. The increased adhesiveness to leukocytes was caused by HCMV replication since endothelial cells exposed to HCMV‐free supernatants and UV‐inactivated HCMV did not show any increase in adhesiveness to any of the leukocytes tested.