Department of Laboratory Medicine, Division of Pathology, Karolinska Institutet and Karolinska University Hospital Huddinge, Stockholm, Sweden.
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
J Infect Dis. 2020 Nov 13;222(12):2041-2051. doi: 10.1093/infdis/jiaa418.
Multiple viruses are implicated in atherosclerosis, but the mechanisms by which they infect cells and contribute to plaque formation in arterial walls are not well understood. Based on reports showing the presence of enterovirus in atherosclerotic plaques we hypothesized that the coxsackievirus and adenovirus receptor (CXADR/CAR), although absent in normal arteries, could be induced during plaque formation. Large-scale microarray and mass spectrometric analyses revealed significant up-regulation of CXADR messenger RNA and protein levels in plaque-invested carotid arteries compared with control arteries. Macrophages were identified as a previously unknown cellular source of CXADR in human plaques and plaques from Ldr-/-Apob100/100 mice. CXADR was specifically associated with M1-polarized macrophages and foam cells and was experimentally induced during macrophage differentiation. Furthermore, it was significantly correlated with receptors for other viruses linked to atherosclerosis. The results show that CXADR is induced in macrophages during plaque formation, suggesting a mechanism by which enterovirus infect cells in atherosclerotic plaques.
多种病毒与动脉粥样硬化有关,但它们感染细胞并促进动脉壁斑块形成的机制尚不清楚。基于报告显示在动脉粥样硬化斑块中存在肠道病毒,我们假设虽然柯萨奇病毒和腺病毒受体 (CXADR/CAR) 在正常动脉中不存在,但在斑块形成过程中可能会被诱导。大规模微阵列和质谱分析显示,与对照动脉相比,斑块浸润的颈总动脉中 CXADR 信使 RNA 和蛋白水平显著上调。巨噬细胞被鉴定为人类斑块和 Ldr-/-Apob100/100 小鼠斑块中 CXADR 的先前未知细胞来源。CXADR 与 M1 极化的巨噬细胞和泡沫细胞特异性相关,并在巨噬细胞分化过程中被实验诱导。此外,它与其他与动脉粥样硬化相关的病毒的受体显著相关。结果表明,CXADR 在斑块形成过程中在巨噬细胞中被诱导,提示肠道病毒感染动脉粥样硬化斑块中细胞的机制。