BACKGROUND: This study investigated neutrophil activation and neutrophil-derived extracellular traps formation in coronary artery ectasia. METHODS: We enrolled 90 patients who underwent coronary angiography, and included 30 patients with coronary artery ectasia (CAE), 30 patients with obstructive coronary artery disease (CAD) and 30 patients with normal coronary arteries (CON). Intra-neutrophil mean myeloperoxidase index (MPXI) was determined using an automated blood cell counter (ADVIA2120 Hematology System). Serum concentrations of plasma adhesion molecules, cytokines, and neutrophil-derived extracellular traps were quantified. RESULTS: The intra-neutrophil mean myeloperoxidase index was reduced in CAE patients compared to CAD and CON patients (1.02â±â3.01, 3.22â±â3.03, 3.52â±â4.25, respectively; CAE vs CAD, pâ=â0.016 and CAE vs CON, pâ=â0.007). Multiple logistic regression analysis showed that MPXI and dsDNA were independent factors that predicted the presence of CAE. CAE patients had higher levels of plasma adhesion molecules (P-selectin glycoprotein ligand-1, E-selectin, L-selectin) and interleukin 1 beta levels. Neutrophil extracellular trap concentrations were significantly higher in the CAE group compared to CAD and CON patients (284.31(258.33-449.91) ng/mL, 225.12(203.34-257.13) ng/mL, and 247.37(231.04-273.01) ng/mL, respectively; CAE vs CAD, pâ=â0.000 and CAE vs CON, pâ=â0.001). CONCLUSIONS: Peripheral neutrophils from CAE patients were activated and neutrophil extracellular traps were elevated in the plasma. IL-1β and soluble adhesion molecules may be the causal factors for neutrophil activation.
Neutrophil activation and neutrophil derived neutrophil extracellular trap formation in patients with coronary artery ectasia.
冠状动脉扩张患者的中性粒细胞活化和中性粒细胞衍生的中性粒细胞胞外陷阱形成
阅读:7
作者:Guo Yuchao, Liu Ruifeng, Chen Lianfeng, Wu Wei, Zhang Shuyang
| 期刊: | BMC Cardiovascular Disorders | 影响因子: | 2.300 |
| 时间: | 2020 | 起止号: | 2020 Mar 2; 20(1):101 |
| doi: | 10.1186/s12872-020-01398-0 | 研究方向: | 细胞生物学 |
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
