通过静电电荷介导单细胞粘附加速动脉样硬化
Ariane Schumski1,2, Almudena Ortega-Gómez1,2, Kanin Wichapong3
1Institute for Cardiovascular Prevention (IPEK), LMU Munich Hospital, Germany (A.S., A.O.-G., C.W., P. Lemnitzer, J.R.V., C.P., L.P.O., J.W., Y.D., O.S.).
Circulation
|November 10, 2020
概括
急性感染通过促进中性粒细胞外陷 (NETs) 加快动脉样硬化. 在NET中,基因组H2a驱动单细胞粘附,在内毒性时增加血管炎症和病变大小.
科学领域:
- 心血管研究
- 免疫学
- 微生物学
背景情况:
- 急性感染是已知的心血管炎症和并发症的危险因素.
- 感染与心血管疾病恶化的确切机制尚不清楚.
- 来自格拉姆阴性细菌的脂多糖 (LPS) 激活了像中性粒细胞这样的免疫细胞,释放了促进炎症的中性粒细胞外陷 (NET).
研究的目的:
- 研究急性感染和随后的中性粒细胞激活如何加速血管炎症.
- 阐明NET在动脉样硬化过程中的作用.
主要方法:
- 在高胆固醇血症小鼠中使用脂多糖注射模拟急性感染.
- 通过对大动脉根的体形测量来评估动脉硬化进展情况.
- 使用静脉内显微镜和体外测试量出了动脉骨髓细胞粘附的数量.
主要成果:
- 治疗LPS增加了动脉样损伤的大小和骨髓细胞积累.
- 在动脉光线上观察到NET沉积,NET抑制减少了病变扩张.
- 在NET中,基因组H2a被确定为以电荷依赖的方式吸引单细胞的关键介质.
结论:
- 与NET相关的基因素H2a驱动了单细胞对NET的电荷依赖粘附.
- 这种过程在急性内毒症中加速动脉样硬化.
- 向H2a是一种潜在的治疗策略,可以缓解感染引起的心血管并发症.
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