Respiratory syncytial virus causes increased bronchial epithelial permeability.
BACKGROUND
Respiratory syncytial virus (RSV)-induced diseases are mediated through active cytokines released during infection. We hypothesized that RSV infection causes bronchial epithelial monolayer permeability in vitro via induction of vascular endothelial growth factor (VEGF).


METHODS
Human bronchial epithelial cells were infected with RSV. In some cultures, VEGF antibody was included to block VEGF response; in other cultures, palivizumab was added to block RSV infection. Permeability was assessed in real-time using electric cell-substrate impedance sensing. VEGF release was assessed using enzyme-linked immunosorbent assay. Gap formation was assessed using live cell imaging.


RESULTS
RSV-infected cells demonstrated a decrease in the resistance of the monolayer indicating an increase in permeability; this increase was blocked with VEGF-specific antibody, and palivizumab. Intercellular gap formation developed in RSV-infected epithelial monolayers.


CONCLUSIONS
RSV increases permeability of the bronchial airway epithelial monolayer via VEGF induction.
Kilani
Muna M
MM
Indiana University Medical Center, Indianapolis, USA.
Mohammed
Kamal A
KA
Nasreen
Najmunnisa
N
Hardwick
Joyce A
JA
Kaplan
Mark H
MH
Tepper
Robert S
RS
Antony
Veena B
VB
D001980:Bronchi / Q000378:metabolism / Q000821:virology*; D002478:Cells, Cultured; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D010539:Permeability; D018357:Respiratory Syncytial Virus Infections / Q000378:metabolism*; D012136:Respiratory Syncytial Viruses; D042442:Vascular Endothelial Growth Factors / Q000096:biosynthesis*
D042442:Vascular Endothelial Growth Factors