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流感病毒感染与炎症细胞因子与急性心肌梗死的关系。

Association of influenza virus infection and inflammatory cytokines with acute myocardial infarction.

机构信息

Department of Laboratory Diagnostics, First Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.

出版信息

Inflamm Res. 2012 Jun;61(6):591-8. doi: 10.1007/s00011-012-0449-3. Epub 2012 Feb 29.

DOI:10.1007/s00011-012-0449-3
PMID:22373653
Abstract

OBJECTIVE

To explore the potential relationship between previous influenza virus (IV) infection and acute myocardial infarction (AMI), and the mechanism of atherosclerosis, we conducted a case-control study and examined inflammatory cytokines to assess the association of previous IV infection and AMI.

METHODS

A questionnaire-based survey was conducted to collect information about demographic characteristics and heart disease risk factors. Fasting blood samples were obtained to measure immunoglobulin (Ig) G antibodies to influenza virus A (IV-A), influenza virus B (IV-B), cytomegalovirus, herpes simplex virus type-1 and type-2, adenovirus, rubella virus and Chlamydia pneumoniae, and to measure the level of certain biochemistry markers: interleukin-2, 6, 10 and 18 (IL-2, 6, 10 and 18), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), endothelin-1 (ET-1), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1).

RESULTS

Compared with the controls, the cases were more likely to have positive IgG antibodies to IV-A and IV-B [IV-A: odds ratio (OR): 3.1, 95% confidence interval (CI): 1.5-6.4; IV-B: OR: 10.2, 95% CI: 5.7-20.0]. After adjustment for potential confounding variables, the risk of AMI was still associated with the presence of IgG antibodies to IV-A (adjusted OR: 5.5, 95% CI: 1.3-23.0) and IV-B (adjusted OR: 20.3, 95% CI: 5.6-40.8). The levels of IL-2, 6, 10 and18, TNF-α, IFN-γ, ET-1, sICAM-1 and sVCAM-1 in patients with AMI were significantly higher than those of the controls (P < 0.01).

CONCLUSIONS

Our study supports the hypothesis that previous IV infection is associated with AMI. Inflammatory cytokines may take part in the development of atherosclerosis and trigger the occurrence of AMI.

摘要

目的

探讨既往流感病毒(IV)感染与急性心肌梗死(AMI)的潜在关系及其与动脉粥样硬化的发生机制。我们进行了一项病例对照研究,并检测了炎症细胞因子,以评估既往 IV 感染与 AMI 的相关性。

方法

采用问卷调查的方式收集人口统计学特征和心脏病危险因素等信息。采集空腹血样,检测流感病毒 A(IV-A)、流感病毒 B(IV-B)、巨细胞病毒、单纯疱疹病毒 1 型和 2 型、腺病毒、风疹病毒和肺炎衣原体的 IgG 抗体,并检测白细胞介素 2、6、10 和 18(IL-2、6、10 和 18)、肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)、内皮素-1(ET-1)、可溶性细胞间黏附分子-1(sICAM-1)和可溶性血管细胞黏附分子-1(sVCAM-1)等生物化学标志物的水平。

结果

与对照组相比,病例组更易出现 IV-A 和 IV-B 的 IgG 抗体阳性[IV-A:比值比(OR):3.1,95%置信区间(CI):1.5-6.4;IV-B:OR:10.2,95%CI:5.7-20.0]。调整潜在混杂因素后,AMI 的发病风险仍与 IV-A(调整 OR:5.5,95%CI:1.3-23.0)和 IV-B(调整 OR:20.3,95%CI:5.6-40.8)的 IgG 抗体阳性相关。AMI 患者的 IL-2、6、10 和 18、TNF-α、IFN-γ、ET-1、sICAM-1 和 sVCAM-1 水平明显高于对照组(P<0.01)。

结论

本研究支持既往 IV 感染与 AMI 相关的假说。炎症细胞因子可能参与动脉粥样硬化的发生,并触发 AMI 的发生。

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