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Neutrophils induce damage to respiratory epithelial cells infected with respiratory syncytial virus
1Dept of Paediatrics, Flinders Medical Centre, Flinders University, SA, Australia.
Abstract:
The mechanisms by which respiratory syncytial virus (RSV) infection induces bronchiolitis and airway disease are unclear. The presence of large numbers of polymorphonuclear leukocytes (PMN) in the airways of infants with RSV infection suggests a potential role of PMN in airway injury associated with RSV infection. To investigate the potential role of neutrophils in RSV bronchiolitis, human alveolar type II cells (A549 cells) were infected with different doses of RSV for 6-48 h. A 51Cr-releasing assay was used to measure PMN-induced damage and image analysis was used to determine PMN adhesion and detachment of epithelial cells. The results showed that RSV infection of epithelial cells enhanced PMN adherence in a dose- and time-dependent pattern, RSV infection alone could damage and detach epithelial cells to a limited extent and PMN significantly augmented RSV infection-induced damage and detachment of epithelial cells. These data suggest that respiratory syncytial virus infection of respiratory epithelial cells enhances neutrophil adhesion to the epithelium and that activated neutrophils augment the damage and detachment of epithelium infected with the virus. Polymorphonuclear leukocytes may contribute to the pathogenesis of respiratory syncytial virus airway disease by inducing epithelial damage and cell loss.
Insights
Respiratory syncytial virus (RSV) infection increases neutrophil adhesion to airway cells. Activated neutrophils then worsen virus-induced epithelial damage, contributing to RSV-related airway disease.
Area of Science:
- Pulmonology
- Virology
- Immunology
Background:
- The precise mechanisms of respiratory syncytial virus (RSV) induced bronchiolitis and airway disease remain incompletely understood.
- The significant presence of polymorphonuclear leukocytes (PMN) in infant airways during RSV infection suggests their potential involvement in airway injury.
Purpose of the Study:
- To investigate the role of neutrophils in the pathogenesis of RSV bronchiolitis.
- To determine if RSV infection enhances neutrophil adherence to respiratory epithelial cells and if neutrophils exacerbate virus-induced epithelial damage.
Main Methods:
- Human alveolar type II cells (A549) were infected with varying doses of RSV over 6-48 hours.
- A 51Cr-releasing assay quantified PMN-induced epithelial cell damage.
- Image analysis assessed PMN adhesion and detachment from epithelial cells.
Main Results:
- RSV infection of epithelial cells significantly enhanced PMN adherence in a dose- and time-dependent manner.
- While RSV infection alone caused limited epithelial damage, PMN markedly augmented this damage and cell detachment.
- RSV infection of respiratory epithelial cells promotes neutrophil adhesion, and activated neutrophils exacerbate virus-induced epithelial damage and cell loss.
Conclusions:
- Neutrophil recruitment and activation play a critical role in the epithelial damage observed in RSV infection.
- Polymorphonuclear leukocytes may contribute significantly to the pathogenesis of RSV-induced airway disease through epithelial injury and cell loss.