Human lungs show limited permissiveness for SARS-CoV-2 due to scarce ACE2 levels but virus-induced expansion of inflammatory macrophages. Katja Hönzke , Benedikt Obermayer , Christin Mache , Diana Fathykova , Mirjana Kessler , Simon Dökel , Emanuel Wyler , Morris Baumgardt , Anna Löwa , Karen Hoffmann , Patrick Graff , Jessica Schulze , Maren Mieth , Katharina Hellwig , Zeynep Demir , Barbara Biere , Linda Brunotte , Angeles Mecate-Zambrano , Judith Bushe , Melanie Dohmen , Christian Hinze , Sefer Elezkurtaj , Mario Tönnies , Torsten T Bauer , Stephan Eggeling , Hong-Linh Tran , Paul Schneider , Jens Neudecker , Jens C Rückert , Kai M Schmidt-Ott , Jonas Busch , Frederick Klauschen , David Horst , Helena Radbruch , Josefine Radke , Frank Heppner , Victor M Corman , Daniela Niemeyer , Marcel A Müller , Christine Goffinet , Ronja Mothes , Anna Pascual-Reguant , Anja Erika Hauser , Dieter Beule , Markus Landthaler , Stephan Ludwig , Norbert Suttorp , Martin Witzenrath , Achim D Gruber , Christian Drosten , Leif-Erik Sander , Thorsten Wolff , Stefan Hippenstiel , Andreas C Hocke The European respiratory journal（2022）
摘要
Collectively, our findings indicate that severe lung injury in COVID-19 likely results from a macrophage triggered immune activation rather than direct viral damage of the alveolar compartment.
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