The Journal of infectious diseases · 2007
Immunopathogenesis of respiratory syncytial virus bronchiolitis.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Bennett Berkeley L, Garofalo Roberto P, Cron Stanley G, Hosakote Yashoda M, Atmar Robert L, Macias Charles G, Piedra Pedro A
Аннотация
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.
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.