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[慢性感染与热休克蛋白在周围动脉疾病中的作用]

[Role of chronic infection and heat shock proteins in peripheral arterial disease].

作者信息

Rabczyński Maciej, Adamiec Rajmund

机构信息

Katedra i Klinika Angiologii, Nadciśnienia Tetniczego i Diabetologii AM, Wrocław.

出版信息

Przegl Lek. 2007;64(6):419-22.

Abstract

The activation of the immunologic system plays an immportant role in the initiation of atherogenesis, as shown in numerous studies. However the role of infectious agents in this process still remains controversial. The aim of this study was to investigate the involvement of heat shock protein as a link between infection and peripheral arterial disease. 31 patients suffering from lower limb ischemia were enrolled in the study. Patients were divided into 2 groups. Group I - patients with peripheral arterial disease, group II patients with diabetic macroangiopathy. The control group consisted of 11 healthy volunteers. Blood samples were taken from each participant in order to determine serum concentrations of anti Chlamydia pneumoniae, CMV and HSP 60/65 antibodies. Statistic analysis showed anti-C. pneumoniae IgG (p< 0.025) and anti-CMV IgG (p<0.0157) antibodies were significantly more frequent in both study groups in comparison with healthy controls. Antibodie levels were also found significantly higher than in controls. Mean concentration of anti-C. pneumoniae IgG in the study group was 69.67574 vs. 18.59722 [AU/ml] in the control group (p<0.01). Analogical anti CMV IgG levels in the study group were 337.6516 vs 121.3778 [AU/ml] in controls (p<0.025). Similar changes in antibody concentration were noticed for the C. pneumoniae IgA index. 0.835258 vs. 0.176333 (p< 0.005). Antibodies against HSP 60/65 were present in significantly higher titre (p<0.005). No significant differences in antibody levels were detected beteween groups I and II. The positive correlation between anti-C. pneumoniae Ig A (r=0.3910; p<0.03) and anti HSP 60/65 antibodies titre, as well as anti-C. pneumoniae Ig G (r= 0.7151; p<0.00009) and anti HSP 60/65 speaks for the heat shock protein involvement in atherosclerotic plaque development.

摘要

如众多研究所示,免疫系统的激活在动脉粥样硬化的起始过程中发挥着重要作用。然而,感染因子在这一过程中的作用仍存在争议。本研究的目的是调查热休克蛋白作为感染与外周动脉疾病之间联系的参与情况。31例下肢缺血患者被纳入研究。患者被分为两组。第一组为外周动脉疾病患者,第二组为糖尿病大血管病变患者。对照组由11名健康志愿者组成。采集每位参与者的血样,以测定抗肺炎衣原体、巨细胞病毒和热休克蛋白60/65抗体的血清浓度。统计分析表明,与健康对照组相比,两个研究组中的抗肺炎衣原体IgG(p<0.025)和抗巨细胞病毒IgG(p<0.0157)抗体明显更常见。抗体水平也显著高于对照组。研究组中抗肺炎衣原体IgG的平均浓度为69.67574,而对照组为18.59722[AU/ml](p<0.01)。研究组中类似的抗巨细胞病毒IgG水平在对照组中为337.6516对121.3778[AU/ml](p<0.025)。肺炎衣原体IgA指数的抗体浓度也有类似变化。0.835258对0.176333(p<0.005)。抗热休克蛋白60/65的抗体滴度明显更高(p<0.005)。在第一组和第二组之间未检测到抗体水平的显著差异。抗肺炎衣原体IgA(r=0.3910;p<0.03)与抗热休克蛋白60/65抗体滴度之间的正相关,以及抗肺炎衣原体IgG(r=0.7151;p<0.00009)与抗热休克蛋白60/65之间的正相关表明热休克蛋白参与了动脉粥样硬化斑块的发展。

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