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Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions
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SARS-CoV-2 targets the lysosome to mediate airway inflammatory cell death

Xiao Sun1, Jun Yu2,3,4, Sunny Hei Wong2,3,5

  • 1Department of Anaesthesia and Intensive Care and Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Administrative Region, China.

Autophagy
|January 24, 2022
PubMed

Insights

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may trigger pyroptosis, a form of inflammatory cell death, by disrupting autophagy. This study investigates SARS-CoV-2

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • The coronavirus disease 2019 (COVID-19) pandemic, caused by SARS-CoV-2, necessitates understanding its pathogenic mechanisms.
  • Autophagy is a crucial innate immune response against viral infections, often manipulated by RNA viruses like SARS-CoV-2.
  • The precise relationship between SARS-CoV-2-induced autophagic dysfunction, cell death, and inflammation remains incompletely understood.

Purpose of the Study:

  • To investigate whether SARS-CoV-2 targets autophagy to induce inflammasome-dependent pyroptosis in lung epithelial cells.
  • To elucidate the role of autophagic flux impairment in SARS-CoV-2-mediated pyroptosis.
  • To explore the potential link between viral-induced autophagy subversion and programmed cell death in COVID-19 pathogenesis.

Main Methods:

  • Utilizing lung epithelial cell models infected with SARS-CoV-2.
  • Assessing autophagic flux and its impairment by SARS-CoV-2 infection.
  • Analyzing inflammasome activation, including caspase 1 (CASP1) and gasdermin D (GSDMD) cleavage.
  • Quantifying pyroptotic cell death markers.

Main Results:

  • SARS-CoV-2 infection leads to the impairment of autophagic flux in lung epithelial cells.
  • Viral non-structural protein 6 (NSP6) is identified as a key factor in disrupting autophagic processes.
  • SARS-CoV-2-induced autophagic impairment activates the NLRP3 inflammasome, leading to CASP1-dependent pyroptosis.
  • GSDMD cleavage and pore formation are observed, indicating the execution of pyroptosis.

Conclusions:

  • SARS-CoV-2 actively subverts autophagy to promote inflammasome activation and pyroptosis in lung epithelial cells.
  • Autophagic flux impairment is a critical mechanism by which SARS-CoV-2 drives inflammatory cell death.
  • Targeting autophagic pathways may represent a therapeutic strategy for managing COVID-19-associated lung injury.
Keywords:
Cell deathCovidNSPlungpyroptosis

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