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首页> 外文期刊>Annals of Clinical and Laboratory Science: Official Journal of the Association of Clinical Scientists >Murine cytomegalovirus infection markedly reduces serum MCP-1 levels in MCP-1 transgenic mice.
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Murine cytomegalovirus infection markedly reduces serum MCP-1 levels in MCP-1 transgenic mice.

机译：小鼠巨细胞病毒感染可明显降低MCP-1转基因小鼠的血清MCP-1水平。

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摘要

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-1beta 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.
机译：单核细胞趋化蛋白-1（MCP-1）是一种促炎性趋化因子，据信在动脉粥样硬化中起主要作用。受损的内皮细胞表达MCP-1，MCP-1将单核细胞吸引到血管壁并导致动脉粥样硬化的形成。巨细胞病毒感染也可能在动脉粥样硬化中发挥作用，并加速过表达MCP-1的组织中的炎症。为了检查巨细胞病毒感染与MCP-1的关系，我们用鼠巨细胞病毒（MCMV）感染了MCP-1转基因小鼠，并在感染后6天收集了血清，以通过ELISA评估TH1相关的细胞因子水平。在MCMV感染后第6天，MCP-1转基因小鼠的血清IL-10，IL-12和IFN-γ水平升高，而IL-1beta和TNF-α的水平却未检测到。但是，与未感染的转基因小鼠相比，MCMV-1转基因小鼠在MCMV感染后MCP-1血清水平降低了> 50％。当对MCP-1转基因小鼠施用M33无效的MCMV时，这种效果并不那么明显。 MCMV降低血清MCP-1水平的机制尚不清楚，但是这种作用可以提高病毒的存活率，从而使CMV有助于动脉粥样硬化的慢性炎症。

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