RSV-induced expanded ciliated cells contribute to bronchial wall thickening

Sattya N. Talukdar, Jaspreet Osan, Ken Ryan, Bryon Grove, Danielle Perley, Bony D. Kumar, Shirley Yang, Sydney Dallman, Lauren Hollingsworth, Kristina L. Bailey, Masfique Mehedi

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


Viral infection, particularly respiratory syncytial virus (RSV), causes inflammation in the bronchiolar airways (bronchial wall thickening, also known as bronchiolitis). This bronchial wall thickening is a common pathophysiological feature in RSV infection, but it causes more fatalities in infants than in children and adults. However, the molecular mechanism of RSV-induced bronchial wall thickening remains unknown, particularly in healthy adults. Using highly differentiated pseudostratified airway epithelium generated from primary human bronchial epithelial cells, we revealed RSV-infects primarily ciliated cells. The infected ciliated cells expanded substantially without compromising epithelial membrane integrity and ciliary functions and contributed to the increased height of the airway epithelium. Furthermore, we identified multiple factors, e.g., cytoskeletal (ARP2/3-complex-driven actin polymerization), immunological (IP10/CXCL10), and viral (NS2), contributing to RSV-induced uneven epithelium height increase in vitro. Thus, RSV-infected expanded cells contribute to a noncanonical inflammatory phenotype, which contributes to bronchial wall thickening in the airway, and is termed cytoskeletal inflammation.

Original languageEnglish (US)
Article number199060
JournalVirus Research
StatePublished - Apr 2 2023


  • ALI
  • ARP2
  • ARP2/3-complex
  • Actin polymerization
  • Bronchial wall thickening
  • Bronchiolitis
  • Cytoskletal inflammation
  • Epithelial height
  • IP10
  • NHBE
  • NS2
  • RSV

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases
  • Cancer Research


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