在SARS-CoV-2感染后进行内皮激活的CXCL10依赖的上皮血管交叉对话
Chaillot Laura1, Blondot Marie-Lise2, Recordon-Pinson Patricia2,3
1BRIC INSERM U1312, Université de Bordeaux, Pessac, 33615, France.
Scientific reports
|July 1, 2025
概括
SARS-CoV-2 感染会通过上皮细胞间接引起血管炎症. 这涉及细胞因子CXCL10,突出显示了一种与COVID-19血管影响相关的新型上皮质-内皮质细胞通信通路.
科学领域:
- 血管生物学 血管生物学
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
背景情况:
- 血管网络受到SARS-CoV-2的重大影响.
- 导致SARS-CoV-2引起血管炎症的机制以及表皮-内皮细胞交叉交谈的作用尚未完全理解.
研究的目的:
- 为了研究SARS-CoV-2与血管系统之间的相互作用.
- 为了确定SARS-CoV-2是否直接感染内皮细胞.
- 阐明表皮-内皮细胞交叉对话在SARS-CoV-2-诱导的血管炎症中的作用.
主要方法:
- 使用了2D和3D血管液体体体外模型.
- 在具有或没有ACE2过度表达的内皮细胞中评估了SARS-CoV-2感染.
- 在上皮细胞感染后分析了内皮细胞的炎症反应.
- 确定了参与细胞间通信的关键细胞因子.
主要成果:
- SARS-CoV-2 没有有效地感染缺乏 ACE2 的内皮细胞.
- 过度表达ACE2的内皮细胞显示病毒吸收率低,没有高效的生产.
- 表皮细胞的感染引发了内皮细胞显著的炎症反应.
- 鉴定出CXCL10是一种关键的促炎细胞因子,它调解了这种交叉对话.
结论:
- SARS-CoV-2主要通过表皮-内皮细胞通信间接影响血管系统.
- CXCL10在调解SARS-CoV-2引起的血管炎症方面发挥着至关重要的作用.
- 结果证实了患者队列中的临床相关性,强调了这种途径在COVID-19病变发生过程中的重要性.
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