生物
2019年冠状病毒病(COVID-19)
地塞米松
单核细胞
2019-20冠状病毒爆发
严重急性呼吸综合征冠状病毒2型(SARS-CoV-2)
大流行
免疫学
病毒学
内科学
疾病
内分泌学
医学
爆发
传染病(医学专业)
作者
Rainer Knoll,Elisa T. Helbig,Kilian Dahm,Olufemi Bolaji,Frederik Hamm,Oliver Dietrich,Martina Van Uelft,Sophie Merit Müller,Lorenzo Bonaguro,Jonas Schulte-Schrepping,L. A. Petrov,Benjamin Krämer,Michael Kraut,Paula Stubbemann,Charlotte Thibeault,Sophia Brumhard,Heidi Theis,Gudrun Hack,Elena De Domenico,Jacob Nattermann
出处
期刊:Cell
[Cell Press]
日期:2024-07-03
卷期号:187 (16): 4318-4335.e20
被引量:11
标识
DOI:10.1016/j.cell.2024.06.014
摘要
Dexamethasone is a life-saving treatment for severe COVID-19, yet its mechanism of action is unknown, and many patients deteriorate or die despite timely treatment initiation. Here, we identify dexamethasone treatment-induced cellular and molecular changes associated with improved survival in COVID-19 patients. We observed a reversal of transcriptional hallmark signatures in monocytes associated with severe COVID-19 and the induction of a monocyte substate characterized by the expression of glucocorticoid-response genes. These molecular responses to dexamethasone were detected in circulating and pulmonary monocytes, and they were directly linked to survival. Monocyte single-cell RNA sequencing (scRNA-seq)-derived signatures were enriched in whole blood transcriptomes of patients with fatal outcome in two independent cohorts, highlighting the potential for identifying non-responders refractory to dexamethasone. Our findings link the effects of dexamethasone to specific immunomodulation and reversal of monocyte dysregulation, and they highlight the potential of single-cell omics for monitoring in vivo target engagement of immunomodulatory drugs and for patient stratification for precision medicine approaches.
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