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J Bacteriol Virol. 2008 Mar;38(1):39-46. Korean. Original Article. https://doi.org/10.4167/jbv.2008.38.1.39
Kim MS , Yi HA , Lee CH .
School of Life Sciences, Chungbuk National University, 410 Seongbong-Ro, Heungduk-Gu, Cheongju, Chungbuk, Korea. chlee@cbu.ac.kr
Institute of Biotechnology, Chungbuk National University, 410 Seongbong-Ro, Heungduk-Gu, Cheongju, Chungbuk, Korea.
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.

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