Journal
CHEST
Volume 126, Issue 1, Pages 186-191Publisher
ELSEVIER
DOI: 10.1378/chest.126.1.186
Keywords
edema; electric cell-substrate impedance sensing; respiratory syncytial virus; vascular endothelial growth factor
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Funding
- NIAID NIH HHS [R01/AI45338-04, R01-AI37454-08] Funding Source: Medline
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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, palivizurnab 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. Conclusion: RSV increases permeability of the bronchial airway epithelial monolayer via VEGF induction.
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