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首页> 外文期刊>Comparative Medicine >Effects of Murine Norovirus on Chlamydia pneumoniae-Accelerated Atherosclerosis in ApoE(-/-) Mice
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Effects of Murine Norovirus on Chlamydia pneumoniae-Accelerated Atherosclerosis in ApoE(-/-) Mice

机译：鼠诺如病毒对ApoE（-/-）小鼠肺炎衣原体加速动脉粥样硬化的影响

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摘要

Chlamydia pneumoniae (Cpn), a common respiratory pathogen of humans, is associated with human cardiovascular disease and the acceleration of atherosclerosis in hyperlipidemic animal models. Our laboratory has demonstrated that murine norovirus (MNV), a prevalent infection of laboratory mice, can unpredictably alter atherosclerosis in hyperlipidemic Ld1r(-/-) and ApoE(-/-) mice. Given that MNV has a tropism for macrophages and may exacerbate atherogenesis, we investigated whether coinfection with MNV and Cpn might alter macrophage phenotypes in vitro and atherosclerosis in ApoE(-/-) mice. In the presence of oxidized low-density lipoprotein, coinfection of ApoE(-/-) bone marrow-derived macrophages (BMDM) with MNV and Cpn resulted in significant increases in gene expression of IL6, MCP1, iNOS, and TNF alpha compared with Cpn-monoinfected BMDM. On the basis of these findings, we hypothesized that concurrent MNV Cpn infection might increase plaque lesion size in vivo. As expected, Cpn monoinfection of ApoE(-/-) mice increased mean plaque size by 62% compared with that in uninfected mice. However, MNV did not significantly alter plaque lesion size in MNV Cpn-coinfected mice compared with Cpn-monoinfected mice. There were no differences in aortic cytokines locally at the site of plaque development or in peritoneal macrophages at 1 wk after infection in MNV Cpn-coinfected mice compared with Cpn-monoinfected mice. MNV was not detected in the aortic tissue of MNV-infected mice at 1 or 8 wk after infection regardless of Cpn status. These data suggest that MNV infection does not appreciably alter plaque development in Cpn-accelerated atherosclerosis in ApoE(-/-) mice.
机译：肺炎衣原体（Cpn）是人类常见的呼吸道病原体，与人类心血管疾病和高脂血症动物模型中动脉粥样硬化的加速有关。我们的实验室已经证明，鼠诺如病毒（MNV）是实验室小鼠的普遍感染，可以不可预测地改变高脂血症Ld1r（-/-）和ApoE（-/-）小鼠的动脉粥样硬化。鉴于MNV对巨噬细胞具有嗜性，并可能加剧动脉粥样硬化，我们调查了MNV和Cpn的共感染是否会改变ApoE（-/-）小鼠的体外巨噬细胞表型和动脉粥样硬化。在氧化的低密度脂蛋白的存在下，ApoE（-/-）骨髓巨噬细胞（BMDM）与MNV和Cpn的共感染导致IL6，MCP1，iNOS和TNFα的基因表达与Cpn相比显着增加-单感染BMDM。基于这些发现，我们假设并发的MNV Cpn感染可能会增加体内斑块病变的大小。正如预期的那样，与未感染的小鼠相比，ApoE（-/-）小鼠的Cpn单次感染使平均噬菌斑大小增加了62％。但是，与Cpn单感染的小鼠相比，MNV在Cpn感染的MNV小鼠中并没有显着改变斑块病变的大小。与Cpn单感染的小鼠相比，MNV Cpn感染的小鼠感染后1周时，斑块发育部位局部的主动脉细胞因子或腹膜巨噬细胞没有差异。无论Cpn状态如何，在感染后1或8周时，在MNV感染小鼠的主动脉组织中均未检测到MNV。这些数据表明，MNV感染不会明显改变ApoE（-/-）小鼠Cpn加速动脉粥样硬化中的斑块发展。

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