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Loss of CFTR Reverses Senescence Hallmarks in SARS-CoV-2 Infected Bronchial Epithelial Cells

Flavia Merigo1, Anna Lagni2, Federico Boschi3

  • 1Anatomy and Histology Section, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37134 Verona, Italy.

International Journal of Molecular Sciences
|June 19, 2024
PubMed

Insights

SARS-CoV-2 infection reversed cellular senescence in cystic fibrosis (CF) cells, unlike in healthy cells. This finding may explain why COVID-19 has a milder impact on CF patients.

Area of Science:

  • Cell Biology
  • Virology
  • Genetics

Background:

  • SARS-CoV-2 infection can induce cellular senescence.
  • Cystic Fibrosis (CF) models show a senescence-like phenotype.
  • Previous studies indicated minimal SARS-CoV-2 impact on CFTR-defective cells.

Purpose of the Study:

  • Investigate senescence hallmarks in SARS-CoV-2 infection within CFTR-defective cells.
  • Compare cellular responses between CFTR-defective and wild-type (WT) cells upon SARS-CoV-2 infection.
  • Elucidate molecular mechanisms behind reduced COVID-19 severity in CF patients.

Main Methods:

  • Infection of WT and CFTR knockout (KO) 16HBE14o- cells with SARS-CoV-2.
  • Analysis of p21 and Ki67 expression via immunohistochemistry.
  • Quantification of viral and p21 gene expression using real-time PCR.
  • Subcellular analysis of lipid accumulation in CFTR KO cells.

Main Results:

  • CFTR KO cells exhibited higher p21 and lower Ki67 expression pre-infection.
  • SARS-CoV-2 infection reversed this trend in CFTR KO cells (low p21, high Ki67) and reduced viral gene expression.
  • WT cells showed activation of senescence pathways upon SARS-CoV-2 infection.
  • Lipid accumulation (lipolysosomes, residual bodies) was observed in CFTR KO cells.

Conclusions:

  • SARS-CoV-2 infection differentially affects senescence pathways in CF and non-CF bronchial epithelial cells.
  • Cellular senescence activation in CFTR-defective cells is reversed by SARS-CoV-2 infection.
  • Findings suggest a potential molecular basis for the reduced clinical impact of COVID-19 in CF patients.
Keywords:
CFTRSARS-CoV-2autophagycystic fibrosislipidlipolysosomesenescenceultrastructure

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