Goblet Cell Hyperplasia Increases SARS-CoV-2 Infection in Chronic Obstructive Pulmonary Disease

Jaspreet Osan, Sattya N. Talukdar, Friederike Feldmann, Beth Ann DeMontigny, Kailey Jerome, Kristina L. Bailey, Heinz Feldmann, Masfique Mehedi

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Chronic obstructive pulmonary disease (COPD) is one of the underlying conditions in adults of any age that place them at risk for developing severe illnesses associated with COVID-19. To determine whether SARS-CoV-2’s cellular tropism plays a critical role in severe pathophysiology in the lung, we investigated its host cell entry receptor distribution in the bronchial airway epithelium of healthy adults and high-risk adults (those with COPD). We found that SARS-CoV-2 preferentially infects goblet cells in the bronchial airway epithelium, as mostly goblet cells harbor the entry receptor angiotensin-converting enzyme 2 (ACE2) and its cofactor transmembrane serine protease 2 (TMPRSS2). We also found that SARS-CoV-2 replication was substantially increased in the COPD bronchial airway epithelium, likely due to COPD-associated goblet cell hyperplasia. Likewise, SARS-CoV and Middle East respiratory syndrome (MERS-CoV) infection increased disease pathophysiology (e.g., syncytium formation) in the COPD bronchial airway epithelium. Our results reveal that goblet cells play a critical role in SARS-CoV-2-induced pathophysiology in the lung.

Original languageEnglish (US)
JournalMicrobiology Spectrum
Volume10
Issue number4
DOIs
StatePublished - Aug 2022

Keywords

  • COPD
  • COVID-19
  • MUC5AC
  • MUC5B
  • SARS-CoV-2
  • air-liquid interface
  • airway epithelium
  • cell sloughing
  • ciliated cells
  • goblet cell hyperplasia
  • goblet cells
  • syncytium

ASJC Scopus subject areas

  • Physiology
  • Ecology
  • Immunology and Microbiology(all)
  • Genetics
  • Microbiology (medical)
  • Cell Biology
  • Infectious Diseases

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