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Wendisch, D.* ; Dietrich, O.* ; Mari, T.* ; von Stillfried, S.* ; Ibarra Del Rio, I.A. ; Mittermaier, M.* ; Mache, C.* ; Chua, R.L.* ; Knöll, R.* ; Timm, S.* ; Brumhard, S.* ; Krammer, T.* ; Zauber, H.* ; Hiller, A.L.* ; Pascual-Reguant, A.* ; Mothes, R.* ; Bülow, R.D.* ; Schulze, J.* ; Leipold, A.M.* ; Djudjaj, S.* ; Erhard, F.* ; Geffers, R.* ; Pott, F.* ; Kazmierski, J.* ; Radke, J.* ; Pergantis, P.* ; Baßler, K.* ; Conrad, C.* ; Aschenbrenner, A.C.* ; Sawitzki, B.* ; Landthaler, M.* ; Wyler, E.* ; Horst, D.* ; Hippenstiel, S.* ; Hocke, A.C.* ; Heppner, F.L.* ; Uhrig, A.* ; Garcia, C.* ; Machleidt, F.* ; Herold, S.* ; Elezkurtaj, S.* ; Thibeault, C.* ; Witzenrath, M.* ; Cochain, C.* ; Suttorp, N.* ; Drosten, C.* ; Goffinet, C.* ; Kurth, F.* ; Schultze, J.L.* ; Radbruch, H.* ; Ochs, M.* ; Eils, R.* ; Müller-Redetzky, H.* ; Hauser, A.E.* ; Luecken, M. ; Theis, F.J. ; Wolff, T.* ; Boor, P.* ; Selbach, M.* ; Saliba, A.E.* ; Sander, L.E.*

SARS-CoV-2 infection triggers profibrotic macrophage responses and lung fibrosis.

Cell 184, 6243-6261.e27 (2021)
Verlagsversion DOI PMC
Free by publisher
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
COVID-19-induced “acute respiratory distress syndrome” (ARDS) is associated with prolonged respiratory failure and high mortality, but the mechanistic basis of lung injury remains incompletely understood. Here, we analyze pulmonary immune responses and lung pathology in two cohorts of patients with COVID-19 ARDS using functional single-cell genomics, immunohistology, and electron microscopy. We describe an accumulation of CD163-expressing monocyte-derived macrophages that acquired a profibrotic transcriptional phenotype during COVID-19 ARDS. Gene set enrichment and computational data integration revealed a significant similarity between COVID-19-associated macrophages and profibrotic macrophage populations identified in idiopathic pulmonary fibrosis. COVID-19 ARDS was associated with clinical, radiographic, histopathological, and ultrastructural hallmarks of pulmonary fibrosis. Exposure of human monocytes to SARS-CoV-2, but not influenza A virus or viral RNA analogs, was sufficient to induce a similar profibrotic phenotype in vitro. In conclusion, we demonstrate that SARS-CoV-2 triggers profibrotic macrophage responses and pronounced fibroproliferative ARDS.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Ards ; Covid-19 ; Fibrosis ; Ipf ; Lung ; Macrophages ; Monocytes ; Proteomics ; Pulmonary Fibrosis ; Sars-cov-2 ; Single-cell Transcriptomics; Extracorporeal Membrane-oxygenation; Idiopathic Pulmonary-fibrosis; Apoptotic Cells; C/ebp-beta; Covid-19; Cytokine; Osteopontin; Receptor; Disease; Protein
ISSN (print) / ISBN 0092-8674
e-ISSN 1097-4172
Zeitschrift Cell
Quellenangaben Band: 184, Heft: 26, Seiten: 6243-6261.e27 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge, Mass.
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Computational Biology (ICB)
Förderungen German Ministry of Education and Research (BMBF)
Deutsche For-schungsgemeinschaft (DFG)
BMBF
Comprehensive Heart Failure Center Wurzburg
German Network University Medicine
DEFEAT PANDEMIcs
OrganoStrat
NAPKON
BMBF CAPSyS
CAPSyS-COVID
SYMPATH
PROVID
RECAST
RAPID-consortia
national research node MSTARS
EU Horizon 2020
European Research Council
Berlin University Alliance
German Registry of COVID-19 Au-topsies (DeRegCOVID)
Federal Ministry of Health (BMG)
Medical Faculty of RWTH Aachen University
Berlin Institute of Health (BIH) PA-COVID-19
Department of Genomics & Immunoregulation at LIMES Institute
IZKF at University Hospital Wurzburg
govern-ment of Bavaria (Bayerische Staatsregierung
Jurgen Manchot Foundation
Germany's Excellence Strategy
BIH-ChariteDigital Clinician Scientist Program