Comprehensive transcriptomic analysis of COVID-19 blood, lung, and airway.
Comprehensive transcriptomic analysis of COVID-19 blood, lung, and airway.
复制标题
DOI：
10.1038/s41598-021-86002-x
复制
发表时间：
2021-03-29
影响因子：
4.6
通讯作者：
Lipsky PE
中科院分区：
文献类型：
--
作者：
Daamen AR;Bachali P;Owen KA;Kingsmore KM;Hubbard EL;Labonte AC;Robl R;Shrotri S;Grammer AC;Lipsky PE
SARS-CoV2是一种以前没有特征的冠状病毒，也是新冠肺炎大流行的病原体。宿主对SARS-CoV2的反应尚未完全描述，这阻碍了精确的治疗方法。为了解决这个问题，我们对新冠肺炎患者的血液、肺和呼吸道的基因表达数据进行了全面的分析。我们的结果表明，新冠肺炎的发病机制是由高度炎症但在每个隔室有不同转录特征的髓系细胞群体驱动的。肺中细胞毒细胞的相对缺乏提示了一种模型，在该模型中，病毒的延迟清除可能允许过度的髓系细胞激活，从而通过产生炎症介质而促进疾病的发病。基因表达谱还确定了可以用现有药物修改的潜在治疗靶点。这些数据表明，转录图谱可以帮助我们了解新冠肺炎在个体患者中的发病机制。
SARS-CoV2 is a previously uncharacterized coronavirus and causative agent of the COVID-19 pandemic. The host response to SARS-CoV2 has not yet been fully delineated, hampering a precise approach to therapy. To address this, we carried out a comprehensive analysis of gene expression data from the blood, lung, and airway of COVID-19 patients. Our results indicate that COVID-19 pathogenesis is driven by populations of myeloid-lineage cells with highly inflammatory but distinct transcriptional signatures in each compartment. The relative absence of cytotoxic cells in the lung suggests a model in which delayed clearance of the virus may permit exaggerated myeloid cell activation that contributes to disease pathogenesis by the production of inflammatory mediators. The gene expression profiles also identify potential therapeutic targets that could be modified with available drugs. The data suggest that transcriptomic profiling can provide an understanding of the pathogenesis of COVID-19 in individual patients.
登录
查看更多内容
DOI：
10.1016/j.ijid.2004.07.014
发表时间：
2005-11
期刊：
International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases
影响因子：
--
作者：
He Z;Zhao C;Dong Q;Zhuang H;Song S;Peng G;Dwyer DE
通讯作者：
Dwyer DE
影响因子：
5.8
作者：
Gu, Zuguang;Eils, Roland;Schlesner, Matthias
通讯作者：
Schlesner, Matthias
影响因子：
8
作者：
Catalina, Michelle D.;Bachali, Prathyusha;Lipsky, Peter E.
通讯作者：
Lipsky, Peter E.
影响因子：
2.6
作者：
Grammer, A. C.;Ryals, M. M.;Lipsky, P. E.
通讯作者：
Lipsky, P. E.
影响因子：
4.6
作者：
Heron, M.;Grutters, J. C.;van Velzen-Blad, H.
通讯作者：
van Velzen-Blad, H.