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Laboratory and Animal Investigations |

Respiratory Syncytial Virus Causes Increased Bronchial Epithelial Permeability*

Muna M. Kilani, MD; Kamal A. Mohammed, PhD; Najmunnisa Nasreen, PhD; Joyce A. Hardwick, BA; Mark H. Kaplan, PhD; Robert S. Tepper, MD, PhD; Veena B. Antony, MD
Author and Funding Information

Affiliations: *From the Indiana University Medical Center, Indianapolis, IN.,  Currently at the Division of Pulmonary & Critical Care Medicine, Department of Medicine, University of Florida, Gainesville, FL.

Correspondence to: Veena Antony, MD, Division of Pulmonary & Critical Care Medicine, Department of Medicine, University of Florida, PO Box 100225, Gainesville, FL 32610-0225; e-mail: antonvb@medicine.ufl.edu



Chest. 2004;126(1):186-191. doi:10.1378/chest.126.1.186
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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, 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.

Conclusion: RSV increases permeability of the bronchial airway epithelial monolayer via VEGF induction.

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