Chronic infections and atherosclerosis

被引:35
作者
Ayada, Kiyoshi [1 ]
Yokata, Kenji [1 ]
Kobayashi, Kazuko [1 ]
Shoenfeld, Yehuda [1 ]
Matsuura, Eiji [1 ]
Oguma, Keiji [1 ]
机构
[1] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Cell Chem, Okayama 7008558, Japan
来源
AUTOIMMUNITY, PT D: AUTOIMMUNE DISEASE, ANNUS MIRABILIS | 2007年 / 1108卷
关键词
anti-heat shock protein (HSP60); atherosclerosis; Helicobacter pylori (H. pylori); HEAT-SHOCK-PROTEIN; CHLAMYDIA-PNEUMONIAE INFECTION; HELICOBACTER-PYLORI INFECTION; IDIOPATHIC THROMBOCYTOPENIC PURPURA; ACUTE MYOCARDIAL-INFARCTION; ACUTE CORONARY SYNDROMES; SERUM ANTIBODIES; HUMAN HEAT-SHOCK-PROTEIN-60; CAROTID ATHEROSCLEROSIS; IMMUNE-RESPONSES;
D O I
10.1196/annals.1422.062
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:594 / 602
页数:9
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