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


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
Issue number4
StatePublished - Aug 2022


  • 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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