德国柏林大学Roland Eils等研究人员合作利用单细胞分析发现,COVID-19严重程度与气道上皮与免疫细胞相互作用有关。相关论文于2020年6月26日在线发表在《自然—生物技术》杂志上。
Title: COVID-19 severity correlates with airway epithelium–immune cell interactions identified by single-cell analysis
Author: Robert Lorenz Chua, Soeren Lukassen, Saskia Trump, Bianca P. Hennig, Daniel Wendisch, Fabian Pott, Olivia Debnath, Loreen Thrmann, Florian Kurth, Maria Theresa Vlker, Julia Kazmierski, Bernd Timmermann, Sven Twardziok, Stefan Schneider, Felix Machleidt, Holger Mller-Redetzky, Melanie Maier, Alexander Krannich, Sein Schmidt, Felix Balzer, Johannes Liebig, Jennifer Loske, Norbert Suttorp, Jrgen Eils, Naveed Ishaque, Uwe Gerd Liebert, Christof von Kalle, Andreas Hocke, Martin Witzenrath, Christine Goffinet, Christian Drosten, Sven Laudi, Irina Lehmann, Christian Conrad, Leif-Erik Sander, Roland Eils
Issue&Volume: 2020-06-26
Abstract: 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.
DOI: 10.1038/s41587-020-0602-4
Source: https://www.nature.com/articles/s41587-020-0602-4
Nature Biotechnology:《自然—生物技术》,创刊于1996年。隶属于施普林格·自然出版集团,最新IF:31.864
官方网址:https://www.nature.com/nbt/
投稿链接:https://mts-nbt.nature.com/cgi-bin/main.plex