Human lungs show limited permissiveness for SARS-CoV-2 due to scarce ACE2 levels but virus-induced expansion of inflammatory macrophages.
Katja HönzkeBenedikt ObermayerChristin MacheDiana FathykovaMirjana KesslerSimon DökelEmanuel WylerMorris BaumgardtAnna LöwaKaren HoffmannPatrick GraffJessica SchulzeMaren MiethKatharina HellwigZeynep DemirBarbara BiereLinda BrunotteAngeles Mecate-ZambranoJudith BusheMelanie DohmenChristian HinzeSefer ElezkurtajMario TönniesTorsten T BauerStephan EggelingHong-Linh TranPaul SchneiderJens NeudeckerJens C RückertKai M Schmidt-OttJonas BuschFrederick KlauschenDavid HorstHelena RadbruchJosefine RadkeFrank L HeppnerVictor Max CormanDaniela NiemeyerMarcel A MüllerChristine GoffinetRonja MothesAnna Pascual-ReguantAnja Erika HauserDieter BeuleMarkus LandthalerStephan LudwigNorbert SuttorpMartin WitzenrathAchim D GruberChristian DrostenLeif-Erik SanderThorsten WolffStefan HippenstielAndreas C HockePublished in: The European respiratory journal (2022)
Collectively, our findings indicate that severe lung injury in COVID-19 probably results from a macrophage-triggered immune activation rather than direct viral damage of the alveolar compartment.