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10.1016/j.stem.2020.09.013

http://scihub22266oqcxt.onion/10.1016/j.stem.2020.09.013
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32979316!7500949!32979316
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suck abstract from ncbi


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pmid32979316      Cell+Stem+Cell 2020 ; 27 (6): 962-973.e7
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  • SARS-CoV-2 Infection of Pluripotent Stem Cell-Derived Human Lung Alveolar Type 2 Cells Elicits a Rapid Epithelial-Intrinsic Inflammatory Response #MMPMID32979316
  • Huang J; Hume AJ; Abo KM; Werder RB; Villacorta-Martin C; Alysandratos KD; Beermann ML; Simone-Roach C; Lindstrom-Vautrin J; Olejnik J; Suder EL; Bullitt E; Hinds A; Sharma A; Bosmann M; Wang R; Hawkins F; Burks EJ; Saeed M; Wilson AA; Muhlberger E; Kotton DN
  • Cell Stem Cell 2020[Dec]; 27 (6): 962-973.e7 PMID32979316show ga
  • A hallmark of severe COVID-19 pneumonia is SARS-CoV-2 infection of the facultative progenitors of lung alveoli, the alveolar epithelial type 2 cells (AT2s). However, inability to access these cells from patients, particularly at early stages of disease, limits an understanding of disease inception. Here, we present an in vitro human model that simulates the initial apical infection of alveolar epithelium with SARS-CoV-2 by using induced pluripotent stem cell-derived AT2s that have been adapted to air-liquid interface culture. We find a rapid transcriptomic change in infected cells, characterized by a shift to an inflammatory phenotype with upregulation of NF-kappaB signaling and loss of the mature alveolar program. Drug testing confirms the efficacy of remdesivir as well as TMPRSS2 protease inhibition, validating a putative mechanism used for viral entry in alveolar cells. Our model system reveals cell-intrinsic responses of a key lung target cell to SARS-CoV-2 infection and should facilitate drug development.
  • |Adenosine Monophosphate/analogs & derivatives/pharmacology[MESH]
  • |Alanine/analogs & derivatives/pharmacology[MESH]
  • |Alveolar Epithelial Cells/*virology[MESH]
  • |Animals[MESH]
  • |Antiviral Agents/pharmacology[MESH]
  • |COVID-19/virology[MESH]
  • |Cells, Cultured[MESH]
  • |Drug Development[MESH]
  • |Enzyme Inhibitors/pharmacology[MESH]
  • |Humans[MESH]
  • |Inflammation/*virology[MESH]
  • |Models, Biological[MESH]
  • |Pluripotent Stem Cells/cytology/virology[MESH]
  • |RNA-Seq[MESH]
  • |SARS-CoV-2/*physiology[MESH]
  • |Serine Endopeptidases/metabolism[MESH]


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