巨细胞病毒感染参与动脉粥样硬化发生的机制

Investigating the Mechanism of Atherogenesis with Cytomegalovirus Infection

探讨巨细胞病毒感染与动脉粥样硬化的相关性及其可能机制。酶联免疫吸附试验检测一个大样本病人血清中的抗人巨细胞病毒的IgG抗体以及C 反应蛋白 ,同时用聚合酶链式反应检测动脉粥样硬化病变中人巨细胞病毒特异性的即时早期基因 ,探讨巨细胞病毒感染和动脉粥样硬化的关系 ;采用反转录聚合酶链式反应检测人巨细胞病毒感染对内皮细胞趋化因子表达的影响。结果发现动脉粥样硬化组血清中的人巨细胞病毒的阳性率显著高于非动脉粥样硬化组 (分别为 82 .2 %和 6 1.0 % ,P =0 .0 2 ) ;动脉粥样硬化患者血清中的C 反应蛋白水平显著高于无动脉粥样硬化的对照组病人 (5 .912± 3.795mg L比 2 .871± 1.76 1mg L ,P =0 .0 0 0 ) ;而且动脉粥样硬化斑块中人巨细胞病毒基因出现率显著高于正常血管组织 (13 15比 2 7,P =0 .0 1)。人巨细胞病毒感染还可上调内皮细胞ECV 30 4表达单核细胞趋化蛋白 1和不规则趋化因子。表明人巨细胞病毒感染参与动脉粥样硬化的形成和发生 ,可能与人巨细胞病毒上调内皮细胞趋化因子表达有关。

Aim To study the relationship between human cytomegalovirus (HCMV) infection and atherogenesis and the putative mechanism. Methods The HCMV IgG and C-reactive protein (CRP) of subject serum and the existence of HCMV immediate early (IE) gene in the atherosclerotic plaque were detected by enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR). The expression of chemokines in endothelial cells after HCMV infection was also studied. Results The positive ratio of HCMV IgG was significantly higher in atherosclerosis group than that in non-atherosclerosis group (82.2% vs 61.0%, P=0.02); the serum CRP level of atherosclerosis group was significantly higher than that of non-atherosclerosis (5.912±3.795 mg/L vs 2.871±1.761 mg/L, P=0.000); HCMV-specific gene in atherosclerotic plaque was much more frequently detected than that in normal vascular tissue (13/15 vs 2/7, P=0.01). HCMV infection could upregulate the expression of chemokines monocyte chemoattractant protein-1 and fractalkine in endothelial cell ECV-304. Conclusions HCMV infection is involved in the pathogenesis of atherosclerosis, which may be mediated by up-regulated expression of chemokines in ECV-304 after HCMV infection.