SARS‐CoV‐2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells
The SARS‐CoV‐2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID‐19 pathogenesis, especially host factors facilitating virus infection and replication. SARS‐CoV‐2 was reported to enter cells via binding to...
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| Vydané v: | The EMBO journal Ročník 39; číslo 10; s. e105114 - n/a |
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| Hlavní autori: | , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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London
Nature Publishing Group UK
18.05.2020
Springer Nature B.V John Wiley and Sons Inc |
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| ISSN: | 0261-4189, 1460-2075, 1460-2075 |
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| Abstract | The SARS‐CoV‐2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID‐19 pathogenesis, especially host factors facilitating virus infection and replication. SARS‐CoV‐2 was reported to enter cells via binding to ACE2, followed by its priming by TMPRSS2. Here, we investigate
ACE2
and
TMPRSS2
expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While
TMPRSS2
is strongly expressed in both tissues, in the subsegmental bronchial branches
ACE2
is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to RHO GTPase function and viral processes suggesting increased vulnerability for SARS‐CoV‐2 infection. Our data provide a rich resource for future investigations of COVID‐19 infection and pathogenesis.
Synopsis
Coronavirus entry requires its binding to host cell receptor ACE2 and subsequent priming by TMPRSS2. Using unpublished single‐cell data of the human lung and bronchia, this study reveals expression of potential SARS‐CoV‐2 cofactors
ACE2
,
TMPRSS2
and
FURIN
primarily in bronchial cells transitioning from secretory to ciliated identity.
Single‐cell dataset comprising 57,229 cells from the lung and subsegmental bronchial branches of 16 human donors was used for studying potential SARS‐CoV‐2 relevant host factors.
In the bronchial epithelium,
ACE2
is most strongly expressed in cells transient secretory cells.
A subset of
ACE2
+
cells co‐expresses the proteases TMPRSS2 and/or FURIN
Trends towards age‐ and sex‐dependent changes in
ACE2
mRNA levels were observed.
Graphical Abstract
A single‐cell RNA‐seq resource identifies expression of coronavirus entry‐linked host cofactors
ACE2
,
TMPRSS2
and
FURIN
primarily in bronchial cells in cells transitioning from secretory to ciliated identity. |
|---|---|
| AbstractList | The SARS‐CoV‐2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID‐19 pathogenesis, especially host factors facilitating virus infection and replication. SARS‐CoV‐2 was reported to enter cells via binding to ACE2, followed by its priming by TMPRSS2. Here, we investigate
ACE2
and
TMPRSS2
expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While
TMPRSS2
is strongly expressed in both tissues, in the subsegmental bronchial branches
ACE2
is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to RHO GTPase function and viral processes suggesting increased vulnerability for SARS‐CoV‐2 infection. Our data provide a rich resource for future investigations of COVID‐19 infection and pathogenesis.
Synopsis
Coronavirus entry requires its binding to host cell receptor ACE2 and subsequent priming by TMPRSS2. Using unpublished single‐cell data of the human lung and bronchia, this study reveals expression of potential SARS‐CoV‐2 cofactors
ACE2
,
TMPRSS2
and
FURIN
primarily in bronchial cells transitioning from secretory to ciliated identity.
Single‐cell dataset comprising 57,229 cells from the lung and subsegmental bronchial branches of 16 human donors was used for studying potential SARS‐CoV‐2 relevant host factors.
In the bronchial epithelium,
ACE2
is most strongly expressed in cells transient secretory cells.
A subset of
ACE2
+
cells co‐expresses the proteases TMPRSS2 and/or FURIN
Trends towards age‐ and sex‐dependent changes in
ACE2
mRNA levels were observed.
Graphical Abstract
A single‐cell RNA‐seq resource identifies expression of coronavirus entry‐linked host cofactors
ACE2
,
TMPRSS2
and
FURIN
primarily in bronchial cells in cells transitioning from secretory to ciliated identity. The SARS‐CoV‐2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID‐19 pathogenesis, especially host factors facilitating virus infection and replication. SARS‐CoV‐2 was reported to enter cells via binding to ACE2, followed by its priming by TMPRSS2. Here, we investigate ACE2 and TMPRSS2 expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While TMPRSS2 is strongly expressed in both tissues, in the subsegmental bronchial branches ACE2 is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to RHO GTPase function and viral processes suggesting increased vulnerability for SARS‐CoV‐2 infection. Our data provide a rich resource for future investigations of COVID‐19 infection and pathogenesis. A single‐cell RNA‐seq resource identifies expression of coronavirus entry‐linked host cofactors ACE2,TMPRSS2 and FURIN primarily in bronchial cells in cells transitioning from secretory to ciliated identity. The SARS‐CoV‐2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID‐19 pathogenesis, especially host factors facilitating virus infection and replication. SARS‐CoV‐2 was reported to enter cells via binding to ACE2, followed by its priming by TMPRSS2. Here, we investigate ACE2 and TMPRSS2 expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While TMPRSS2 is strongly expressed in both tissues, in the subsegmental bronchial branches ACE2 is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to RHO GTPase function and viral processes suggesting increased vulnerability for SARS‐CoV‐2 infection. Our data provide a rich resource for future investigations of COVID‐19 infection and pathogenesis. Synopsis Coronavirus entry requires its binding to host cell receptor ACE2 and subsequent priming by TMPRSS2. Using unpublished single‐cell data of the human lung and bronchia, this study reveals expression of potential SARS‐CoV‐2 cofactors ACE2, TMPRSS2 and FURIN primarily in bronchial cells transitioning from secretory to ciliated identity. Single‐cell dataset comprising 57,229 cells from the lung and subsegmental bronchial branches of 16 human donors was used for studying potential SARS‐CoV‐2 relevant host factors. In the bronchial epithelium, ACE2 is most strongly expressed in cells transient secretory cells. A subset of ACE2+ cells co‐expresses the proteases TMPRSS2 and/or FURIN Trends towards age‐ and sex‐dependent changes in ACE2 mRNA levels were observed. A single‐cell RNA‐seq resource identifies expression of coronavirus entry‐linked host cofactors ACE2, TMPRSS2 and FURIN primarily in bronchial cells in cells transitioning from secretory to ciliated identity. The SARS‐CoV‐2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID‐19 pathogenesis, especially host factors facilitating virus infection and replication. SARS‐CoV‐2 was reported to enter cells via binding to ACE2, followed by its priming by TMPRSS2. Here, we investigate ACE2 and TMPRSS2 expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While TMPRSS2 is strongly expressed in both tissues, in the subsegmental bronchial branches ACE2 is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to RHO GTPase function and viral processes suggesting increased vulnerability for SARS‐CoV‐2 infection. Our data provide a rich resource for future investigations of COVID‐19 infection and pathogenesis. The SARS-CoV-2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID-19 pathogenesis, especially host factors facilitating virus infection and replication. SARS-CoV-2 was reported to enter cells via binding to ACE2, followed by its priming by TMPRSS2. Here, we investigate ACE2 and TMPRSS2 expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While TMPRSS2 is strongly expressed in both tissues, in the subsegmental bronchial branches ACE2 is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to RHO GTPase function and viral processes suggesting increased vulnerability for SARS-CoV-2 infection. Our data provide a rich resource for future investigations of COVID-19 infection and pathogenesis.The SARS-CoV-2 pandemic affecting the human respiratory system severely challenges public health and urgently demands for increasing our understanding of COVID-19 pathogenesis, especially host factors facilitating virus infection and replication. SARS-CoV-2 was reported to enter cells via binding to ACE2, followed by its priming by TMPRSS2. Here, we investigate ACE2 and TMPRSS2 expression levels and their distribution across cell types in lung tissue (twelve donors, 39,778 cells) and in cells derived from subsegmental bronchial branches (four donors, 17,521 cells) by single nuclei and single cell RNA sequencing, respectively. While TMPRSS2 is strongly expressed in both tissues, in the subsegmental bronchial branches ACE2 is predominantly expressed in a transient secretory cell type. Interestingly, these transiently differentiating cells show an enrichment for pathways related to RHO GTPase function and viral processes suggesting increased vulnerability for SARS-CoV-2 infection. Our data provide a rich resource for future investigations of COVID-19 infection and pathogenesis. |
| Author | Trefzer, Timo Lukassen, Soeren Hennig, Bianca P Kahn, Nicolas C Kreuter, Michael Muley, Thomas Eils, Roland Chua, Robert Lorenz Boots, Agnes W Winter, Hauke Conrad, Christian Veith, Carmen Schneider, Marc A Meister, Michael |
| AuthorAffiliation | 6 Department of Thoracic Surgery Thoraxklinik, Heidelberg University Hospital Heidelberg Germany 8 Faculty of Health, Medicine and Life Sciences Department of Pharmacology and Toxicology NUTRIM School of Nutrition Translational Research and Metabolism Maastricht University Maastricht the Netherlands 1 Charité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health Berlin Germany 4 Translational Lung Research Center Heidelberg (TLRC) Member of the German Center for Lung Research (DZL) Heidelberg Germany 2 Center for Digital Health Berlin Institute of Health (BIH) Berlin Germany 3 Department of Pneumology and Respiratory Critical Care Medicine Center for interstitial and rare lung diseases Thoraxklinik, Heidelberg University Hospital Heidelberg Germany 7 Division of Redox Regulation German Cancer Research Center (DKFZ) Heidelberg Germany 9 Health Data Science Unit Heidelberg University Hospital and BioQuant Heide |
| AuthorAffiliation_xml | – name: 2 Center for Digital Health Berlin Institute of Health (BIH) Berlin Germany – name: 4 Translational Lung Research Center Heidelberg (TLRC) Member of the German Center for Lung Research (DZL) Heidelberg Germany – name: 3 Department of Pneumology and Respiratory Critical Care Medicine Center for interstitial and rare lung diseases Thoraxklinik, Heidelberg University Hospital Heidelberg Germany – name: 1 Charité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health Berlin Germany – name: 8 Faculty of Health, Medicine and Life Sciences Department of Pharmacology and Toxicology NUTRIM School of Nutrition Translational Research and Metabolism Maastricht University Maastricht the Netherlands – name: 5 Translational Research Unit Thoraxklinik, Heidelberg University Hospital Heidelberg Germany – name: 6 Department of Thoracic Surgery Thoraxklinik, Heidelberg University Hospital Heidelberg Germany – name: 7 Division of Redox Regulation German Cancer Research Center (DKFZ) Heidelberg Germany – name: 9 Health Data Science Unit Heidelberg University Hospital and BioQuant Heidelberg Germany |
| Author_xml | – sequence: 1 givenname: Soeren orcidid: 0000-0001-7045-6327 surname: Lukassen fullname: Lukassen, Soeren organization: Charité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health, Center for Digital Health, Berlin Institute of Health (BIH) – sequence: 2 givenname: Robert Lorenz surname: Chua fullname: Chua, Robert Lorenz organization: Charité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health, Center for Digital Health, Berlin Institute of Health (BIH) – sequence: 3 givenname: Timo surname: Trefzer fullname: Trefzer, Timo organization: Charité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health, Center for Digital Health, Berlin Institute of Health (BIH) – sequence: 4 givenname: Nicolas C surname: Kahn fullname: Kahn, Nicolas C organization: Department of Pneumology and Respiratory Critical Care Medicine, Center for interstitial and rare lung diseases, Thoraxklinik, Heidelberg University Hospital, Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL) – sequence: 5 givenname: Marc A surname: Schneider fullname: Schneider, Marc A organization: Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL), Translational Research Unit, Thoraxklinik, Heidelberg University Hospital – sequence: 6 givenname: Thomas surname: Muley fullname: Muley, Thomas organization: Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL), Translational Research Unit, Thoraxklinik, Heidelberg University Hospital – sequence: 7 givenname: Hauke surname: Winter fullname: Winter, Hauke organization: Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL), Department of Thoracic Surgery, Thoraxklinik, Heidelberg University Hospital – sequence: 8 givenname: Michael surname: Meister fullname: Meister, Michael organization: Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL), Translational Research Unit, Thoraxklinik, Heidelberg University Hospital – sequence: 9 givenname: Carmen surname: Veith fullname: Veith, Carmen organization: Division of Redox Regulation, German Cancer Research Center (DKFZ) – sequence: 10 givenname: Agnes W surname: Boots fullname: Boots, Agnes W organization: Faculty of Health, Medicine and Life Sciences, Department of Pharmacology and Toxicology, NUTRIM School of Nutrition, Translational Research and Metabolism, Maastricht University – sequence: 11 givenname: Bianca P surname: Hennig fullname: Hennig, Bianca P organization: Charité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health, Center for Digital Health, Berlin Institute of Health (BIH) – sequence: 12 givenname: Michael orcidid: 0000-0003-4402-2159 surname: Kreuter fullname: Kreuter, Michael email: kreuter@uni-heidelberg.de organization: Department of Pneumology and Respiratory Critical Care Medicine, Center for interstitial and rare lung diseases, Thoraxklinik, Heidelberg University Hospital – sequence: 13 givenname: Christian orcidid: 0000-0001-7036-342X surname: Conrad fullname: Conrad, Christian email: christian.conrad@bihealth.de organization: Charité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health – sequence: 14 givenname: Roland orcidid: 0000-0002-0034-4036 surname: Eils fullname: Eils, Roland email: roland.eils@bihealth.de organization: Charité ‐ Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, and Berlin Institute of Health, Center for Digital Health, Berlin Institute of Health (BIH), Health Data Science Unit, Heidelberg University Hospital and BioQuant |
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| Keywords | FURIN Human Cell Atlas COVID‐19 epithelial differentiation respiratory tract COVID-19 |
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| SubjectTerms | ACE2 Adult Aging Angiotensin-Converting Enzyme 2 Binding Bronchi - cytology Bronchi - metabolism Cell differentiation Cells, Cultured Chronic Disease - epidemiology Cofactors Coronavirus Infections - genetics Coronaviruses COVID-19 EMBO09 EMBO10 EMBO23 Epithelial Cells - metabolism epithelial differentiation Epithelium Female FURIN Gene Expression Gene Expression Profiling Gene sequencing Germany Goblet Cells - metabolism Guanosine triphosphatases Human Cell Atlas Humans Infections Lung - cytology Lung - metabolism Lungs Male Middle Aged mRNA Nuclei (cytology) Pandemics Pathogenesis Peptidyl-Dipeptidase A - genetics Pneumonia, Viral - genetics Priming Public health Receptors Reference Standards Resource Respiratory system respiratory tract Sequence Analysis, RNA Serine Endopeptidases - genetics Severe acute respiratory syndrome Severe acute respiratory syndrome coronavirus 2 Sex Characteristics Single-Cell Analysis Smoking Tissue Banks Viral diseases Viruses |
| Title | SARS‐CoV‐2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells |
| URI | https://link.springer.com/article/10.15252/embj.20105114 https://onlinelibrary.wiley.com/doi/abs/10.15252%2Fembj.20105114 https://www.ncbi.nlm.nih.gov/pubmed/32246845 https://www.proquest.com/docview/2403840028 https://www.proquest.com/docview/2386280997 https://pubmed.ncbi.nlm.nih.gov/PMC7232010 |
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