Human Cytomegalovirus Induces Intercellular Adhesion Molecule-1 Expression in a Monocytic Cell Line, THP-1.
- Author:
Mi Suk KIM
1
;
Hyun Ah YI
;
Chan Hee LEE
Author Information
- Publication Type:Original Article
- Keywords: HCMV; Inflammation; ICAM-1; NF-kappaB
- MeSH: Cell Line; Cyclooxygenase 2; Cytomegalovirus; Endothelial Cells; Flavonoids; Hepatitis; Humans; Inflammation; Intercellular Adhesion Molecule-1; Monocytes; NF-kappa B; Nitrobenzenes; Pneumonia; Proline; Retinitis; Sulfonamides; Thiocarbamates; Viruses
- From:Journal of Bacteriology and Virology 2008;38(1):39-46
- CountryRepublic of Korea
- Language:Korean
- Abstract: It has been reported that inflammatory diseases such as pneumonitis, retinitis, and hepatitis are associated with human cytomegalovirus (HCMV). Intercellular adhesion molecule (ICAM)-1 is an important inflammatory mediator, helping monocytes adhere to endothelial cells when tissues are infected by pathogen including the HCMV. However, little is known about the mechanism of ICAM-1 stimulation by the HCMV infection in monocytes. In this study, a monocytic cell line THP-1 was used to understand ICAM-1 expression by the HCMV infection. Flow cytometric analyses demonstrated that ICAM-1 was stimulated by the HCMV in THP-1 cells with maximum at 24 hours post infection. The stimulated ICAM-1 expression was dependent on the amount of input virus. In order to understand the mechanism of ICAM-1 stimulation during the HCMV infection, cells were treated with specific inhibitors of key elements in inflammation: NF-kappaB inhibitor PDTC, cyclooxygenase 2 inhibitor NS398, and MEK inhibitor PD98059. Flow cytometric analyses revealed that ICAM-1 expression was decreased when treated with PDTC, but not with NS398 or PD98059. Thus, it is suggested that HCMV-induced ICAM-1 expression in THP-1 cells is associates with NF-kappaB.
