Murine cytomegalovirus infection markedly reduces serum MCP-1 levels in MCP-1 transgenic mice

    Authors

    M. K. Froberg; D. Dannen; A. Adams; J. Parker-Thornburg;P. Kolattukudy

    Comments

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    Abbreviated Journal Title

    Ann. Clin. Lab. Sci.

    Keywords

    cytomegalovirus; atherosclerosis; monocyte chemoattractant protein-1; cytokines; MONOCYTE CHEMOATTRACTANT PROTEIN-1; LOW-DENSITY-LIPOPROTEIN; MUSCLE-CELL; MIGRATION; DEFICIENT MICE; CC CHEMOKINES; ATHEROSCLEROSIS; EXPRESSION; INDUCTION; IL-10; GENE; Medical Laboratory Technology

    Abstract

    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-alpha were increased in MCP-1 transgenic mice on day 6 following MCMV infection, while levels of IL-1 beta 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.

    Journal Title

    Annals of Clinical and Laboratory Science

    Volume

    36

    Issue/Number

    2

    Publication Date

    1-1-2006

    Document Type

    Article

    Language

    English

    First Page

    179

    Last Page

    184

    WOS Identifier

    WOS:000237603400010

    ISSN

    0091-7370

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