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血清热休克蛋白65抗体与临界高血压的关联。

Association of serum antibodies to heat-shock protein 65 with borderline hypertension.

作者信息

Frostegård J, Lemne C, Andersson B, van der Zee R, Kiessling R, de Faire U

机构信息

Department of Medicine, Karolinska Hospital, Stockholm, Sweden.

出版信息

Hypertension. 1997 Jan;29(1 Pt 1):40-4. doi: 10.1161/01.hyp.29.1.40.

DOI:10.1161/01.hyp.29.1.40
PMID:9039077
Abstract

Heat-shock proteins protect cells from damage but are also often the target of immune responses in inflammation and may therefore both induce and perpetuate the chronic inflammation characterizing atherosclerosis. Hypertension is a well-established risk factor for atherosclerosis, and recently, borderline hypertension also has been related to atherosclerosis. The present study investigated the possible role of heat-shock proteins in borderline hypertension and their relation to atherosclerosis by investigating antibody titers against the 65-kD heat-shock protein (HSP65). Sixty-six men with borderline hypertension and 67 age-matched normotensive men (diastolic pressure, 85 to 94 and < 80 mm Hg, respectively) were recruited from a population screening program. Titers of antibodies to HSP65 were determined by enzyme-linked immunosorbent assay. The presence of carotid atherosclerosis was determined by B-mode ultrasonography. Twenty-seven individuals had atherosclerotic plaques: 48 were smokers (more than one to two cigarettes per day). Borderline hypertensive men had higher anti-HSP65 reactivity than normotensive control subjects (P = .034). Smokers with atherosclerosis had low levels of antibodies to HSP65 compared with nonsmokers with atherosclerosis (P = .002). Furthermore, when high-risk individuals (borderline hypertension plus plaque, n = 15) were compared with matched low-risk individuals (normotensive with no plaque, n = 15), the high-risk men had significantly enhanced antibody titers to HSP65 (P = .041). In conclusion, we demonstrate that serum antibody titers to HSP65 are enhanced in individuals with borderline hypertension, which may indicate an ongoing immune reaction in the artery wall.

摘要

热休克蛋白可保护细胞免受损伤,但在炎症过程中也常常是免疫反应的靶点,因此可能既引发又维持动脉粥样硬化所特有的慢性炎症。高血压是动脉粥样硬化公认的危险因素,近来,临界高血压也与动脉粥样硬化相关。本研究通过检测针对65-kD热休克蛋白(HSP65)的抗体滴度,探讨热休克蛋白在临界高血压中的可能作用及其与动脉粥样硬化的关系。从一项人群筛查项目中招募了66名临界高血压男性和67名年龄匹配的血压正常男性(舒张压分别为85至94 mmHg和<80 mmHg)。采用酶联免疫吸附测定法测定HSP65抗体滴度。通过B型超声检查确定颈动脉粥样硬化的存在。27人有动脉粥样硬化斑块;48人吸烟(每天超过1至2支香烟)。临界高血压男性的抗HSP65反应性高于血压正常的对照受试者(P = 0.034)。与有动脉粥样硬化的非吸烟者相比,有动脉粥样硬化的吸烟者的HSP65抗体水平较低(P = 0.002)。此外,当将高危个体(临界高血压加斑块,n = 15)与匹配的低危个体(血压正常且无斑块,n = 15)进行比较时,高危男性的HSP65抗体滴度显著升高(P = 0.041)。总之,我们证明临界高血压个体中血清HSP65抗体滴度升高,这可能表明动脉壁中存在持续的免疫反应。

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