Chronic infections and atherosclerosis
Chronic infections and atherosclerosis
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DOI：
10.1196/annals.1422.062
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发表时间：
2007-01-01
期刊：
影响因子：
--
通讯作者：
Oguma, Keiji
中科院分区：
文献类型：
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作者：
Ayada, Kiyoshi;Yokata, Kenji;Oguma, Keiji
慢性感染引起的免疫炎症过程被认为是决定性的动脉粥样硬化过程之一。特别是抗热休克蛋白抗体与冠心病或脑梗塞等疾病的发生有关，是动脉粥样硬化引起的此外，循环中HSP 60特异性T淋巴细胞的存在可能增加动脉粥样硬化的风险。我们最近证实了幽门螺杆菌感染诱导apoe（+/-）Idlr（+/-）小鼠动脉粥样硬化的证据，并且幽门螺杆菌-抗热休克蛋白特异性Th 1-显性免疫应答在动脉粥样硬化的进展中具有重要作用。这些细胞免疫应答由于分子模拟而引起针对内源性HSP 60（在血管内皮的应激细胞上表达）的自身免疫。因此，用抗生素或用调节Th 1诱导的抗HSP 60抗体进行适当的治疗可以充分地减少动脉粥样硬化的进展。
Immunoinflammatory processes due to chronic infection are thought to be one of the definitive atherogenetic processes. Especially, anti-heat shock protein antibodies have been related to the prevalence of disease such as coronary artery disease or cerebral infarction, etc., resulted from atherosclerosis. Furthermore, the presence of HSP60specific T lymphocytes in circulation may increase the risk of atherosclerosis. We have recently demonstrated the evidences that Helicobacter pylori infection induced atherosclerosis in apoe(+/-)Idlr(+/-) mice and that Hp-anti-heat-shock protein specific Th1-dominant immune responses had a major involvement in the progression of atherosclerosis. These cellular immune responses caused autoimmunity against endogenous HSP60 (expressed on the stressed cells of vascular endothelium), due to the molecular mimicry. Therefore, an appropriate treatment with antibiotics or with anti-HSP60 antibodies, which regulates the Th1 induction, could sufficiently reduce the progression of atherosclerosis.