在致命的COVID-19中,衰老和肺部免疫反应失调导致致命的COVID-19
Natália de Souza Xavier Costa1, Jôse Mara de Brito1,2, Carla Froio1
1Laboratório de Patologia Ambiental e Experimental, Departamento de Patologia, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil.
衰老通过改变肺组织的反应加剧了COVID-19的严重程度. 老年人表现出炎症和纤维化标志物的增加,导致COVID-19严重肺部感染的结果更差.
科学领域:
- 免疫学和老年学
- 传染病的病理学 传染病的病理学
背景情况:
- 老年人经历了不成比例的高COVID-19死亡率,超过80%的死亡发生在60岁以上的人群中.
- 老年人的细胞衰老和炎症可能会增加像COVID-19这样的病毒感染的易感性和严重性.
- 有限的研究已经探索了严重的COVID-19中特定于年龄的肺组织反应.
研究的目的:
- 调查与年龄相关的先天性/获得性免疫和肺组织细胞衰老的变化.
- 为了确定老年肺部如何应对严重的COVID-19感染.
- 为了确定与年龄相关的COVID-19严重程度相关的特定分子标记.
主要方法:
- 从已故个人 (COVID-19和非肺原因) 的肺组织分析,按年龄分类 (<60岁和≥60岁).
- 免疫组织化学评估19种标记物 (免疫细胞,COVID-19受体,细胞因子,衰老标记物).
- 卢米内克斯多重检测测量COVID-19肺组织中的25种细胞因子/化学因子.
主要成果:
- 与年龄相匹配的对照组相比,老年COVID-19患者在CD8+T细胞,IFN-α2,TLR7,pSTAT-3,p21和p53表达方面表现出显著差异.
- 在老年COVID-19患者和年轻成年人中观察到IFN-α2和TGF-β的更高蛋白质表达.
- 在较老的COVID-19肺部观察到CD20+细胞密度下降的趋势,以及较短的症状至死亡间隔.
结论:
- 肺组织与年龄相关的变化会对COVID-19的易感性和严重程度产生不利影响.
- 衰老促进肺部的炎症和亲纤维性反应,加剧了COVID-19的结果.
- 老年肺部的特定免疫和衰老标志物对于了解COVID-19的病原性至关重要.
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