Regulation of cellular immunity prevents Helicobacter pylori-induced atherosclerosis
Regulation of cellular immunity prevents Helicobacter pylori-induced atherosclerosis
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DOI：
10.1177/0961203309106600
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发表时间：
2009-11-01
期刊：
影响因子：
2.6
通讯作者：
Oguma, K.
中科院分区：
文献类型：
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作者：
Ayada, K.;Yokota, K.;Oguma, K.
幽门螺杆菌（H.幽门螺杆菌（pylori）是不仅引起胃十二指肠疾病而且引起消化道外疾病的主要病原体。在这项研究中，我们证明了H。pylori感染促进了杂合子apoe（+/-）ldlr（+/-）小鼠动脉粥样硬化的形成。雄性小鼠从6周龄开始用高脂饲料喂养。在16周龄时，在H中观察到动脉粥样硬化病变的发展。pylori感染的小鼠，并且似乎与针对H.幽门螺杆菌源热休克蛋白60（Hp-HSP 60）和T细胞跨内皮迁移的增加。用Hp-HSP 60或H.用抗生素根除幽门螺杆菌显著降低了动脉粥样硬化的进展，伴随着Th 1分化的下降和它们在内皮外的趋化性的降低。因此，口腔感染H. pylori可加速小鼠动脉粥样硬化的发生，Hp-HSP 60主动免疫或根除H.幽门螺杆菌与抗生素可以缓和/预防细胞免疫，从而减少动脉粥样硬化。Lupus（2009）18，1154-1168.
Helicobacter pylori (H. pylori) is a predominant pathogen that causes not only gastroduodenal diseases but also extra-alimentary tract diseases. In this study, we demonstrated that H. pylori infection promoted atherogenesis in heterozygous apoe(+/-) ldlr(+/-) mice. The male mice were fed with high fat diet from the age of 6 weeks. At the age of 16 weeks, development of atherosclerotic lesions was observed in the H. pylori-infected mice, and it seemed to be associated with an elevation of Th1-immune response against H. pylori origin-heat shock protein 60 (Hp-HSP60) and an increment of transendothelial migration of T cells. Subcutaneous immunisation with Hp-HSP60 or H. pylori eradication with antibiotics significantly reduced the progression of atherosclerosis, accompanied by a decline of Th1 differentiation and reduction of their chemotaxis beyond the endothelium. Thus, oral infection with H. pylori accelerates atherosclerosis in mice and the active immunisation with Hp-HSP60 or the eradication of H. pylori with antibiotics can moderate/prevent cellular immunity, resulting in a reduction of atherosclerosis. Lupus (2009) 18, 1154-1168.