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

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SARS-CoV-2 infection triggers profibrotic macrophage responses and lung fibrosis. / Wendisch, Daniel; Dietrich, Oliver; Mari, Tommaso; von Stillfried, Saskia; Ibarra, Ignacio L; Mittermaier, Mirja; Mache, Christin; Chua, Robert Lorenz; Knoll, Rainer; Timm, Sara; Brumhard, Sophia; Krammer, Tobias; Zauber, Henrik; Hiller, Anna Luisa; Pascual-Reguant, Anna; Mothes, Ronja; Bülow, Roman David; Schulze, Jessica; Leipold, Alexander M; Djudjaj, Sonja; Erhard, Florian; Geffers, Robert; Pott, Fabian; Kazmierski, Julia; Radke, Josefine; Pergantis, Panagiotis; Baßler, Kevin; Conrad, Claudia; Aschenbrenner, Anna C; Sawitzki, Birgit; Landthaler, Markus; Wyler, Emanuel; Horst, David; Hippenstiel, Stefan; Hocke, Andreas; Heppner, Frank L; Uhrig, Alexander; Garcia, Carmen; Machleidt, Felix; Herold, Susanne; Elezkurtaj, Sefer; Thibeault, Charlotte; Witzenrath, Martin; Cochain, Clément; Suttorp, Norbert; Drosten, Christian; Goffinet, Christine; Kurth, Florian; Schultze, Joachim L; Radbruch, Helena; Ochs, Matthias; Eils, Roland; Müller-Redetzky, Holger; Hauser, Anja E; Luecken, Malte D; Theis, Fabian J; Conrad, Christian; Wolff, Thorsten; Boor, Peter; Selbach, Matthias; Saliba, Antoine-Emmanuel; Sander, Leif Erik; Deutsche COVID-19 OMICS Initiative (DeCOI).

In: CELL, Vol. 184, No. 26, 22.12.2021, p. 6243-6261.e27.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Wendisch, D, Dietrich, O, Mari, T, von Stillfried, S, Ibarra, IL, Mittermaier, M, Mache, C, Chua, RL, Knoll, R, Timm, S, Brumhard, S, Krammer, T, Zauber, H, Hiller, AL, Pascual-Reguant, A, Mothes, R, Bülow, RD, Schulze, J, Leipold, AM, Djudjaj, S, Erhard, F, Geffers, R, Pott, F, Kazmierski, J, Radke, J, Pergantis, P, Baßler, K, Conrad, C, Aschenbrenner, AC, Sawitzki, B, Landthaler, M, Wyler, E, Horst, D, Hippenstiel, S, Hocke, A, Heppner, FL, 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, JL, Radbruch, H, Ochs, M, Eils, R, Müller-Redetzky, H, Hauser, AE, Luecken, MD, Theis, FJ, Conrad, C, Wolff, T, Boor, P, Selbach, M, Saliba, A-E, Sander, LE & Deutsche COVID-19 OMICS Initiative (DeCOI) 2021, 'SARS-CoV-2 infection triggers profibrotic macrophage responses and lung fibrosis', CELL, vol. 184, no. 26, pp. 6243-6261.e27. https://doi.org/10.1016/j.cell.2021.11.033

APA

Wendisch, D., Dietrich, O., Mari, T., von Stillfried, S., Ibarra, I. L., Mittermaier, M., Mache, C., Chua, R. L., Knoll, 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., ... Deutsche COVID-19 OMICS Initiative (DeCOI) (2021). SARS-CoV-2 infection triggers profibrotic macrophage responses and lung fibrosis. CELL, 184(26), 6243-6261.e27. https://doi.org/10.1016/j.cell.2021.11.033

Vancouver

Wendisch D, Dietrich O, Mari T, von Stillfried S, Ibarra IL, Mittermaier M et al. SARS-CoV-2 infection triggers profibrotic macrophage responses and lung fibrosis. CELL. 2021 Dec 22;184(26):6243-6261.e27. https://doi.org/10.1016/j.cell.2021.11.033

Bibtex

@article{d9e4d07957764e4a9952585750755b2a,
title = "SARS-CoV-2 infection triggers profibrotic macrophage responses and lung fibrosis",
abstract = "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.",
keywords = "Antigens, CD/metabolism, Antigens, Differentiation, Myelomonocytic/metabolism, COVID-19/diagnostic imaging, Cell Communication, Cohort Studies, Fibroblasts/pathology, Gene Expression Regulation, Humans, Idiopathic Pulmonary Fibrosis/diagnostic imaging, Macrophages/pathology, Mesenchymal Stem Cells/pathology, Phenotype, Proteome/metabolism, Receptors, Cell Surface/metabolism, Respiratory Distress Syndrome/diagnostic imaging, SARS-CoV-2/physiology, Tomography, X-Ray Computed, Transcription, Genetic",
author = "Daniel Wendisch and Oliver Dietrich and Tommaso Mari and {von Stillfried}, Saskia and Ibarra, {Ignacio L} and Mirja Mittermaier and Christin Mache and Chua, {Robert Lorenz} and Rainer Knoll and Sara Timm and Sophia Brumhard and Tobias Krammer and Henrik Zauber and Hiller, {Anna Luisa} and Anna Pascual-Reguant and Ronja Mothes and B{\"u}low, {Roman David} and Jessica Schulze and Leipold, {Alexander M} and Sonja Djudjaj and Florian Erhard and Robert Geffers and Fabian Pott and Julia Kazmierski and Josefine Radke and Panagiotis Pergantis and Kevin Ba{\ss}ler and Claudia Conrad and Aschenbrenner, {Anna C} and Birgit Sawitzki and Markus Landthaler and Emanuel Wyler and David Horst and Stefan Hippenstiel and Andreas Hocke and Heppner, {Frank L} and Alexander Uhrig and Carmen Garcia and Felix Machleidt and Susanne Herold and Sefer Elezkurtaj and Charlotte Thibeault and Martin Witzenrath and Cl{\'e}ment Cochain and Norbert Suttorp and Christian Drosten and Christine Goffinet and Florian Kurth and Schultze, {Joachim L} and Helena Radbruch and Matthias Ochs and Roland Eils and Holger M{\"u}ller-Redetzky and Hauser, {Anja E} and Luecken, {Malte D} and Theis, {Fabian J} and Christian Conrad and Thorsten Wolff and Peter Boor and Matthias Selbach and Antoine-Emmanuel Saliba and Sander, {Leif Erik} and {Deutsche COVID-19 OMICS Initiative (DeCOI)}",
note = "Copyright {\textcopyright} 2021. Published by Elsevier Inc.",
year = "2021",
month = dec,
day = "22",
doi = "10.1016/j.cell.2021.11.033",
language = "English",
volume = "184",
pages = "6243--6261.e27",
journal = "CELL",
issn = "0092-8674",
publisher = "Cell Press",
number = "26",

}

RIS

TY - JOUR

T1 - SARS-CoV-2 infection triggers profibrotic macrophage responses and lung fibrosis

AU - Wendisch, Daniel

AU - Dietrich, Oliver

AU - Mari, Tommaso

AU - von Stillfried, Saskia

AU - Ibarra, Ignacio L

AU - Mittermaier, Mirja

AU - Mache, Christin

AU - Chua, Robert Lorenz

AU - Knoll, Rainer

AU - Timm, Sara

AU - Brumhard, Sophia

AU - Krammer, Tobias

AU - Zauber, Henrik

AU - Hiller, Anna Luisa

AU - Pascual-Reguant, Anna

AU - Mothes, Ronja

AU - Bülow, Roman David

AU - Schulze, Jessica

AU - Leipold, Alexander M

AU - Djudjaj, Sonja

AU - Erhard, Florian

AU - Geffers, Robert

AU - Pott, Fabian

AU - Kazmierski, Julia

AU - Radke, Josefine

AU - Pergantis, Panagiotis

AU - Baßler, Kevin

AU - Conrad, Claudia

AU - Aschenbrenner, Anna C

AU - Sawitzki, Birgit

AU - Landthaler, Markus

AU - Wyler, Emanuel

AU - Horst, David

AU - Hippenstiel, Stefan

AU - Hocke, Andreas

AU - Heppner, Frank L

AU - Uhrig, Alexander

AU - Garcia, Carmen

AU - Machleidt, Felix

AU - Herold, Susanne

AU - Elezkurtaj, Sefer

AU - Thibeault, Charlotte

AU - Witzenrath, Martin

AU - Cochain, Clément

AU - Suttorp, Norbert

AU - Drosten, Christian

AU - Goffinet, Christine

AU - Kurth, Florian

AU - Schultze, Joachim L

AU - Radbruch, Helena

AU - Ochs, Matthias

AU - Eils, Roland

AU - Müller-Redetzky, Holger

AU - Hauser, Anja E

AU - Luecken, Malte D

AU - Theis, Fabian J

AU - Conrad, Christian

AU - Wolff, Thorsten

AU - Boor, Peter

AU - Selbach, Matthias

AU - Saliba, Antoine-Emmanuel

AU - Sander, Leif Erik

AU - Deutsche COVID-19 OMICS Initiative (DeCOI)

N1 - Copyright © 2021. Published by Elsevier Inc.

PY - 2021/12/22

Y1 - 2021/12/22

N2 - 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.

AB - 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.

KW - Antigens, CD/metabolism

KW - Antigens, Differentiation, Myelomonocytic/metabolism

KW - COVID-19/diagnostic imaging

KW - Cell Communication

KW - Cohort Studies

KW - Fibroblasts/pathology

KW - Gene Expression Regulation

KW - Humans

KW - Idiopathic Pulmonary Fibrosis/diagnostic imaging

KW - Macrophages/pathology

KW - Mesenchymal Stem Cells/pathology

KW - Phenotype

KW - Proteome/metabolism

KW - Receptors, Cell Surface/metabolism

KW - Respiratory Distress Syndrome/diagnostic imaging

KW - SARS-CoV-2/physiology

KW - Tomography, X-Ray Computed

KW - Transcription, Genetic

U2 - 10.1016/j.cell.2021.11.033

DO - 10.1016/j.cell.2021.11.033

M3 - SCORING: Journal article

C2 - 34914922

VL - 184

SP - 6243-6261.e27

JO - CELL

JF - CELL

SN - 0092-8674

IS - 26

ER -