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COVID-19 诱导的细胞外基质沉积比 ARDS 的其他原因更为明显
Natália de Souza Xavier Costa1, Gabriel Ribeiro Júnior1, Ellen Caroline Toledo do Nascimento1
1Departamento de Patologia (LIM 05), Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
Respiratory research
|November 14, 2023
概括
与其他ARDS原因相比,致命的COVID-19肺组织显示原和TGF-β沉积增加. 这表明,异常的细胞外基质组合有助于严重的COVID-19幸存者的肺部异常.
科学领域:
- 肺部病理学 肺部病理学
- 在COVID-19研究研究中.
- 细胞外矩阵生物学 细胞外矩阵生物学
背景情况:
- 肺纤维化是严重的COVID-19患者需要机械通风 (MV) 的重要问题.
- 在严重的COVID-19肺部中,确切的细胞外基质 (ECM) 组成及其与其他ARDS病因学的区别仍然不清楚.
- 肺部异常在COVID-19幸存者中很普遍,需要更深入地了解潜在的病理学.
研究的目的:
- 为了调查和比较致命的COVID-19病例中的肺 ECM 组成与其他导致ARDS的原因.
- 分析TGF-β的表达及其与COVID-19肺中的ECM元素和细胞因子的相关性.
- 阐明导致COVID-19后肺部异常的病理基质.
主要方法:
- 从28例致命的COVID-19病例和27例非COVID-19ARDS病例的肺组织中量化ECM元素和TGF-β表达.
- 基于机械通风 (MV) 持续时间 (≤6天与≥7天) 的比较.
- 在COVID-19病例中,ECM元素与肺转录组学和细胞因子概况的相关性分析.
主要成果:
- 与非COVID-19 ARDS相比,COVID-19肺部显示出显著更高的原,纤维素,维西卡和TGF-β沉积,与非COVID-19 ARDS相比,其色密度降低.
- 在COVID-19患者中,早期 (≤6天MV) 观察到TGF-β升高.
- 肺原蛋白水平在女性COVID-19患者中较高,基因表达转移表明MV期间改变了纤维化和ECM重塑.
结论:
- 致命的COVID-19的特点是早期的TGF-β表达和MV发病后的ECM组装失调.
- 不受控制的ECM过程导致COVID-19中突出的原沉积,与其他ARDS原因不同.
- 这些发现为COVID-19幸存者肺部异常高患病率提供了病理见解.
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