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10.1016/j.stem.2020.11.010

http://scihub22266oqcxt.onion/10.1016/j.stem.2020.11.010
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33259798!7670932!33259798
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suck abstract from ncbi

pmid33259798      Cell+Stem+Cell 2020 ; 27 (6): 869-875.e4
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  • Direct Exposure to SARS-CoV-2 and Cigarette Smoke Increases Infection Severity and Alters the Stem Cell-Derived Airway Repair Response #MMPMID33259798
  • Purkayastha A; Sen C; Garcia G Jr; Langerman J; Shia DW; Meneses LK; Vijayaraj P; Durra A; Koloff CR; Freund DR; Chi J; Rickabaugh TM; Mulay A; Konda B; Sim MS; Stripp BR; Plath K; Arumugaswami V; Gomperts BN
  • Cell Stem Cell 2020[Dec]; 27 (6): 869-875.e4 PMID33259798show ga
  • Current smoking is associated with increased risk of severe COVID-19, but it is not clear how cigarette smoke (CS) exposure affects SARS-CoV-2 airway cell infection. We directly exposed air-liquid interface (ALI) cultures derived from primary human nonsmoker airway basal stem cells (ABSCs) to short term CS and then infected them with SARS-CoV-2. We found an increase in the number of infected airway cells after CS exposure with a lack of ABSC proliferation. Single-cell profiling of the cultures showed that the normal interferon response was reduced after CS exposure with infection. Treatment of CS-exposed ALI cultures with interferon beta-1 abrogated the viral infection, suggesting one potential mechanism for more severe viral infection. Our data show that acute CS exposure allows for more severe airway epithelial disease from SARS-CoV-2 by reducing the innate immune response and ABSC proliferation and has implications for disease spread and severity in people exposed to CS.
  • |COVID-19/genetics/immunology/*physiopathology/therapy[MESH]
  • |Cells, Cultured[MESH]
  • |Down-Regulation[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]
  • |Interferon-beta/therapeutic use[MESH]
  • |Patient Acuity[MESH]
  • |Respiratory Mucosa/*physiopathology/virology[MESH]
  • |Smoking/*adverse effects[MESH]


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