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,Matthias Becker,Marc Beyer,David Hillus,Philipp Georg,Constantin Loers,Janina Tiedemann,Pinkus Tober‐Lau,Lena J. Lippert,Belén Millet Pascual-Leone,Frank Tacke,Gernot Rohde,Norbert Suttorp,Martin Witzenrath,Antoine‐Emmanuel Saliba,Thomas Ulas,Julia K. Polansky,Birgit Sawitzki,Leif Erik Sander,Joachim L. Schultze,Anna C. Aschenbrenner,Florian Kurth
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.