Chua, Robert Lorenz
Lukassen, Soeren
Trump, Saskia
Hennig, Bianca P.
Wendisch, Daniel
Pott, Fabian
Debnath, Olivia
Thürmann, Loreen
Kurth, Florian
Völker, Maria Theresa
Kazmierski, Julia
Timmermann, Bernd
Timmermann, Bernd
Twardziok, Sven
Schneider, Stefan
Machleidt, Felix
Müller-Redetzky, Holger
Maier, Melanie
Krannich, Alexander
Schmidt, Sein
Balzer, Felix
Liebig, Johannes
Loske, Jennifer
Suttorp, Norbert
Eils, Jürgen
Ishaque, Naveed
Liebert, Uwe Gerd
von Kalle, Christof
Hocke, Andreas
Witzenrath, Martin
Goffinet, Christine
Drosten, Christian
Laudi, Sven
Lehmann, Irina
Conrad, Christian
Sander, Leif Erik
Eils, Roland
2020-07-17T22:40:50Z
2020-07-17T22:40:50Z
2020-06-26
1546-1696
https://www.nature.com/articles/s41587-020-0602-4
http://hdl.handle.net/20.500.12010/10816
25 páginas
application/pdf
Science Direct
reponame:Expeditio Repositorio Institucional UJTL
instname:Universidad de Bogotá Jorge Tadeo Lozano
Interacción de células
COVID-19 severity correlates with airway epithelium–immune cell interactions identified by single-cell analysis
Artículo
Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
info:eu-repo/semantics/openAccess
info:eu-repo/semantics/acceptedVersion
Cell interactions
https://doi.org/10.1038/s41587-020-0602-4
To investigate the immune response and mechanisms associated with severe coronavirus disease 2019 (COVID-19), we performed single-cell RNA sequencing on nasopharyngeal and bronchial samples from 19 clinically well-characterized patients with moderate or critical disease and from five healthy controls. We identified airway epithelial cell types and states vulnerable to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In patients with COVID-19, epithelial cells showed an average three-fold increase in expression of the SARS-CoV-2 entry receptor ACE2, which correlated with interferon signals by immune cells. Compared to moderate cases, critical cases exhibited stronger interactions between epithelial and immune cells, as indicated by ligand–receptor expression profiles, and activated immune cells, including inflammatory macrophages expressing CCL2, CCL3, CCL20, CXCL1, CXCL3, CXCL10, IL8, IL1B and TNF. The transcriptional differences in critical cases compared to moderate cases likely contribute to clinical observations of heightened inflammatory tissue damage, lung injury and respiratory failure. Our data suggest that pharmacologic inhibition of the CCR1 and/or CCR5 pathways might suppress immune hyperactivation in critical COVID-19.