TY - JOUR
T1 - RSV-induced expanded ciliated cells contribute to bronchial wall thickening
AU - Talukdar, Sattya N.
AU - Osan, Jaspreet
AU - Ryan, Ken
AU - Grove, Bryon
AU - Perley, Danielle
AU - Kumar, Bony D.
AU - Yang, Shirley
AU - Dallman, Sydney
AU - Hollingsworth, Lauren
AU - Bailey, Kristina L.
AU - Mehedi, Masfique
N1 - Publisher Copyright:
© 2023
PY - 2023/4/2
Y1 - 2023/4/2
N2 - 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.
AB - 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.
KW - ALI
KW - ARP2
KW - ARP2/3-complex
KW - Actin polymerization
KW - Bronchial wall thickening
KW - Bronchiolitis
KW - Cytoskletal inflammation
KW - Epithelial height
KW - IP10
KW - NHBE
KW - NS2
KW - RSV
UR - http://www.scopus.com/inward/record.url?scp=85147946552&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85147946552&partnerID=8YFLogxK
U2 - 10.1016/j.virusres.2023.199060
DO - 10.1016/j.virusres.2023.199060
M3 - Article
C2 - 36746339
AN - SCOPUS:85147946552
SN - 0168-1702
VL - 327
JO - Virus Research
JF - Virus Research
M1 - 199060
ER -