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Annals of Clinical & Laboratory Science 36:179-184 (2006)
© 2006 Association of Clinical Scientists

Murine Cytomegalovirus Infection Markedly Reduces Serum MCP-1 Levels in MCP-1 Transgenic Mice

M. Kent Froberg1, Devon Dannen1, Alice Adams1, Jan Parker-Thornburg2 and Pappachan Kolattukudy3
1 Department of Pathology, University of Minnesota Duluth School of Medicine, Duluth, Minnesota2 Genetically Engineered Mouse Facility, MD Anderson Cancer Center, Houston, Texas3 Burnett College of Biomedical Sciences, University of Central Florida, Orlando, Florida

Address correspondence to M. Kent Froberg, M.D., Department of Pathology, School of Medicine, University of Minnesota Duluth, 1035 University Drive, Duluth, MN 58812, USA; tel 218 726 7223; fax 218 726 7559; e-mail kfroberg{at}d.umn.edu.

Monocyte chemoattractant protein-1 (MCP-1) is a pro-inflammatory chemokine believed to play a major role in atherogenesis. Injured endothelial cells express MCP-1, which attracts monocytes to the blood vessel wall and leads to the formation of atheromas. Cytomegalovirus infection may also play a role in atherogenesis and accelerates inflammation in tissues that overexpress MCP-1. To examine the relationship of cytomegalovirus infection and MCP-1, we infected MCP-1 transgenic mice with murine cytomegalovirus (MCMV) and collected serum 6 days post-infection to evaluate TH1-related cytokine levels by ELISA. Serum levels of IL-10, IL-12 and IFN-{gamma} were increased in MCP-1 transgenic mice on day 6 following MCMV infection, while levels of IL-1ß and TNF-{alpha} were undetectable. However, MCP-1 serum levels were reduced >50% in MCP-1 transgenic mice following MCMV infection compared to uninfected transgenic mice. This effect was not as dramatic when an M33 null MCMV was administered to MCP-1 transgenic mice. The mechanism by which MCMV lowers serum MCP-1 levels is unknown, but this effect may enhance the survival of the virus and thus allow CMV to contribute to the chronic inflammation of atherogenesis.

Keywords: cytomegalovirus, atherosclerosis, monocyte chemoattractant protein-1, cytokines






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