SARS-CoV-2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells.
Identifieur interne : 000264 ( Main/Merge ); précédent : 000263; suivant : 000265SARS-CoV-2 receptor ACE2 and TMPRSS2 are primarily expressed in bronchial transient secretory cells.
Auteurs : Soeren Lukassen [Allemagne] ; Robert Lorenz Chua [Allemagne] ; Timo Trefzer [Allemagne] ; Nicolas C. Kahn [Allemagne] ; Marc A. Schneider [Allemagne] ; Thomas Muley [Allemagne] ; Hauke Winter [Allemagne] ; Michael Meister [Allemagne] ; Carmen Veith [Allemagne] ; Agnes W. Boots [Pays-Bas] ; Bianca P. Hennig [Allemagne] ; Michael Kreuter [Allemagne] ; Christian Conrad [Allemagne] ; Roland Eils [Allemagne]Source :
- The EMBO journal [ 1460-2075 ] ; 2020.
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.
DOI: 10.15252/embj.20105114
PubMed: 32246845
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<country xml:lang="fr">Allemagne</country>
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<author><name sortKey="Schneider, Marc A" sort="Schneider, Marc A" uniqKey="Schneider M" first="Marc A" last="Schneider">Marc A. Schneider</name>
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<wicri:regionArea>Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL), Heidelberg</wicri:regionArea>
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<author><name sortKey="Muley, Thomas" sort="Muley, Thomas" uniqKey="Muley T" first="Thomas" last="Muley">Thomas Muley</name>
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<author><name sortKey="Winter, Hauke" sort="Winter, Hauke" uniqKey="Winter H" first="Hauke" last="Winter">Hauke Winter</name>
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<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL), Heidelberg</wicri:regionArea>
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<author><name sortKey="Meister, Michael" sort="Meister, Michael" uniqKey="Meister M" first="Michael" last="Meister">Michael Meister</name>
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<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Translational Lung Research Center Heidelberg (TLRC), Member of the German Center for Lung Research (DZL), Heidelberg</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Karlsruhe</region>
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<author><name sortKey="Veith, Carmen" sort="Veith, Carmen" uniqKey="Veith C" first="Carmen" last="Veith">Carmen Veith</name>
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<author><name sortKey="Boots, Agnes W" sort="Boots, Agnes W" uniqKey="Boots A" first="Agnes W" last="Boots">Agnes W. Boots</name>
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<country xml:lang="fr" wicri:curation="lc">Pays-Bas</country>
<wicri:regionArea>Faculty of Health, Medicine and Life Sciences, Department of Pharmacology and Toxicology, NUTRIM School of Nutrition, Translational Research and Metabolism, Maastricht University, Maastricht</wicri:regionArea>
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<author><name sortKey="Hennig, Bianca P" sort="Hennig, Bianca P" uniqKey="Hennig B" first="Bianca P" last="Hennig">Bianca P. Hennig</name>
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<wicri:regionArea>Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin</wicri:regionArea>
<placeName><region type="land" nuts="3">Berlin</region>
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<author><name sortKey="Kreuter, Michael" sort="Kreuter, Michael" uniqKey="Kreuter M" first="Michael" last="Kreuter">Michael Kreuter</name>
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<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Pneumology and Respiratory Critical Care Medicine, Center for interstitial and rare lung diseases, Thoraxklinik, Heidelberg University Hospital, Heidelberg</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Karlsruhe</region>
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<author><name sortKey="Conrad, Christian" sort="Conrad, Christian" uniqKey="Conrad C" first="Christian" last="Conrad">Christian Conrad</name>
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<wicri:regionArea>Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin</wicri:regionArea>
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<author><name sortKey="Eils, Roland" sort="Eils, Roland" uniqKey="Eils R" first="Roland" last="Eils">Roland Eils</name>
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<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin</wicri:regionArea>
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<front><div type="abstract" xml:lang="en">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.</div>
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