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生物芯片谱分析在肺栓塞中促炎细胞因子的上调作用。

Upregulation of Inflammatory Cytokines in Pulmonary Embolism Using Biochip-Array Profiling.

机构信息

Department of Pathology and Laboratory Medicine, Cardiovascular Research Institute, Hemostasis and Thrombosis Research Division, Loyola University Medical Center, Health Sciences Division, Maywood, IL, USA.

Advanced Heart Failure, Mechanical Circulatory Support, Heart Transplant, Jefferson Heart Institute, Sidney Kimmel School of Medicine, Thomas Jefferson University, Philadelphia, PA, USA.

出版信息

Clin Appl Thromb Hemost. 2021 Jan-Dec;27:10760296211013107. doi: 10.1177/10760296211013107.

Abstract

The complex pathophysiology of pulmonary embolism (PE) involves hemostatic activation, inflammatory processes, cellular dysfunction, and hemodynamic derangements. Due to the heterogeneity of this disease, risk stratification and diagnosis remains challenging. Biochip-array technology provides an integrated high throughput method for analyzing blood plasma samples for the simultaneous measurement of multiple biomarkers for potential risk stratification. Using biochip-array method, this study aimed to quantify the inflammatory biomarkers such as interleukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, vascular endothelial growth factor (VEGF), interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and epidermal growth factor (EGF) in 109 clinically confirmed PE patients in comparison to the control group comprised of plasma samples collected from 48 healthy subjects. Cytokines IL-4, IL-6, IL-8, IL-10, IL-1β, and MCP-1 demonstrated varying level of significant increase ( < 0.05) in massive-risk PE patients compared to submassive- and low-risk PE patients. The upregulation of inflammatory cytokines in PE patients observed in this study suggest that inflammation plays an important role in the overall pathophysiology of this disease. The application of biochip-array technology may provide a useful approach to evaluate these biomarkers to understand the pathogenesis and risk stratification of PE patients.

摘要

肺栓塞(PE)的复杂病理生理学涉及止血激活、炎症过程、细胞功能障碍和血液动力学紊乱。由于这种疾病的异质性,风险分层和诊断仍然具有挑战性。生物芯片阵列技术提供了一种集成的高通量方法,用于分析血浆样本,以同时测量多个生物标志物,用于潜在的风险分层。本研究使用生物芯片阵列方法,旨在定量炎症生物标志物,如白细胞介素(IL)-1α、IL-1β、IL-2、IL-4、IL-6、IL-8、IL-10、血管内皮生长因子(VEGF)、干扰素γ(IFN-γ)、肿瘤坏死因子α(TNF-α)、单核细胞趋化蛋白-1(MCP-1)和表皮生长因子(EGF),比较了 109 例临床确诊的 PE 患者与对照组,对照组由 48 名健康受试者的血浆样本组成。与亚大面积和低危 PE 患者相比,大量风险 PE 患者的细胞因子 IL-4、IL-6、IL-8、IL-10、IL-1β和 MCP-1 表现出不同程度的显著增加(<0.05)。本研究中观察到的 PE 患者中炎症细胞因子的上调表明炎症在该疾病的整体病理生理学中起着重要作用。生物芯片阵列技术的应用可能为评估这些生物标志物提供有用的方法,以了解 PE 患者的发病机制和风险分层。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fe8/8113361/c03de719ea01/10.1177_10760296211013107-fig1.jpg

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