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An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
Immunopathogenesis of respiratory syncytial virus bronchiolitis
Berkeley L Bennett1, Roberto P Garofalo, Stanley G Cron
1Department of Pediatrics, Division of Emergency Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA. ppiedra@bcm.tmc.edu.
Insights
Respiratory syncytial virus (RSV) bronchiolitis triggers a strong inflammatory response but does not worsen disease severity. Specific cytokine and chemokine levels may protect against hypoxia in infants.
Area of Science:
- Pediatric Infectious Diseases
- Immunology
- Respiratory Medicine
Background:
- Bronchiolitis is a common childhood respiratory illness, often caused by respiratory syncytial virus (RSV).
- The role of inflammatory mediators in RSV bronchiolitis severity is not fully understood.
- Understanding the relationship between viral infections, cytokines, and disease outcomes is crucial for pediatric respiratory care.
Purpose of the Study:
- To investigate the association between respiratory syncytial virus (RSV) infection and concentrations of cytokines and chemokines.
- To determine the impact of these inflammatory factors on the severity of bronchiolitis in children.
- To differentiate the inflammatory response in RSV versus non-RSV bronchiolitis.
Main Methods:
- Prospective enrollment of children under 24 months with bronchiolitis symptoms in an emergency department.
- Analysis of nasal-wash samples for viral pathogens, including RSV quantification.
- Measurement of cytokine and chemokine levels, correlating them with disease severity indicators like hospitalization and oxygen therapy duration.
Main Results:
- Out of 101 children, 63 had RSV, 13 had other viruses, and 22 had no detected virus.
- RSV bronchiolitis showed a heightened inflammatory response compared to non-RSV cases, but not increased disease severity.
- Interleukin (IL)-6, IL-8, IL-10, interferon (IFN)-gamma, and macrophage inflammatory protein (MIP)-1beta levels were inversely correlated with supplemental oxygen therapy duration.
Conclusions:
- The significant inflammatory response in RSV bronchiolitis does not correlate with increased disease severity.
- Elevated levels of IL-6, IL-8, IFN-gamma, MIP-1beta, and IL-10 may offer protection against hypoxia in bronchiolitis.
- These findings suggest a potential protective role for certain inflammatory mediators in managing RSV bronchiolitis.
Background:
The objective of this study was to elucidate the relation between respiratory syncytial virus (RSV) infection and cytokine/chemokine concentrations, as well as the impact that these factors have on the severity of bronchiolitis.
Methods:
Children <24 months old who presented to the emergency department with clinical symptoms of bronchiolitis were prospectively enrolled in the study. Nasal-wash samples were analyzed to identify viral pathogens and to quantify RSV and cytokine/chemokine concentrations. Severe cases of disease were defined as those requiring hospitalization, and severity was further determined on the basis of the duration of supplemental-oxygen and/or intravenous-fluid therapy.
Results:
A total of 101 children were enrolled, 63 of whom were infected with RSV and 13 of whom were infected with other respiratory viruses; in 22 children, no virus was detected. RSV bronchiolitis was associated with a greater inflammatory response than was non-RSV bronchiolitis, although RSV infection was not associated with more-severe disease. Levels of interleukin (IL)-6, IL-8, IL-10, interferon (IFN)-gamma, and macrophage inflammatory protein (MIP)-1beta were significantly inversely correlated with the duration of supplemental-oxygen therapy.
Conclusion:
The robust inflammatory response associated with RSV infection does not contribute to the severity of RSV bronchiolitis any more than it contributes to the severity of non-RSV bronchiolitis. Elevated levels of proinflammatory mediators IL-6, IL-8, IFN-gamma, and MIP-1beta, as well as of the regulatory cytokine IL-10, may be protective against hypoxia in bronchiolitis.
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