通过患者血刺激的血液透的芯片容器重复了COVID-19中的内皮活化和微血栓形成
Huub J Weener1, Thijs F van Haaps2,3, Ruben W J van Helden4
1Department of Bioengineering Technologies, University of Twente, Enschede, The Netherlands. H.J.Weener@utwente.nl.
Lab on a chip
|March 4, 2025
概括
在严重的COVID-19患者中,由血因素驱动的全身炎症会导致内皮功能障碍和血块形成. 这项研究使用了一种新型芯片模型来证明这些效应,为新疗法铺平了道路.
科学领域:
- 心血管生物学 心血管生物学
- 免疫学 免疫学 免疫学
- 病理生理学 病理生理学
背景情况:
- 严重的COVID-19涉及急性肺损伤,内皮功能障碍和微血栓症,系统性炎症被怀疑是关键贡献者.
- 患者血中的循环炎症因素与严重的COVID-19表型有关.
研究的目的:
- 调查COVID-19患者血中的系统性炎症因素是否可以直接诱导内皮功能障碍和随后的血栓炎症.
- 利用微流体容器芯片模型模拟体内环境,用于研究COVID-19病理生理学.
主要方法:
- 使用人类诱导的多能干干细胞衍生的内皮细胞 (hiPSC-ECs) 建立了微流体容器芯片模型.
- 该模型用住院COVID-19患者的血和人类全血刺激.
- 分析了内皮细胞激活,血小板聚合和中性粒细胞细胞外陷 (NETosis) 的形成.
主要成果:
- 与健康对照组相比,COVID-19患者的血含有较高的炎症性细胞因子.
- 暴露于COVID-19血激活了hiPSC-ECs,升调炎症标记物和病毒防御的转录组模式.
- 在芯片模型中,COVID-19血诱导了血小板聚合的增加和部分NETosis.
结论:
- 血传播的炎症因素在严重的COVID-19中驱动血栓炎症中起着因果作用.
- 船舶上芯片模型是未来对严重COVID-19的诊断,预防和治疗研究的一个有价值的工具.
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