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The Enhancement or Prevention of Airway Hyperresponsiveness during Reinfection with Respiratory Syncytial Virus Is Critically Dependent on the Age at First Infection and IL-13 Production

 Azzeddine Dakhama  ;  Jung-Won Park  ;  Christian Taube  ;  Anthony Joetham  ;  Annette Balhorn  ;  Nobuaki Miyahara  ;  Katsuyuki Takeda  ;  Erwin W. Gelfand 
 Journal of Immunology, Vol.175(3) : 1876-1883, 2005 
Journal Title
 Journal of Immunology 
Issue Date
Aging/immunology* ; Animals ; Animals, Newborn/immunology* ; Animals, Newborn/virology* ; Bronchial Hyperreactivity/immunology* ; Bronchial Hyperreactivity/physiopathology* ; Bronchial Hyperreactivity/prevention & control ; Disease Models, Animal ; Disease Susceptibility/immunology ; Disease Susceptibility/physiopathology ; Eosinophilia/immunology ; Eosinophilia/physiopathology ; Eosinophilia/virology ; Interleukin-13/biosynthesis* ; Interleukin-13/physiology ; Mice ; Mice, Inbred BALB C ; Recurrence ; Respiratory Syncytial Virus Infections/immunology* ; Respiratory Syncytial Virus Infections/physiopathology* ; Respiratory Syncytial Virus Infections/prevention & control ; Weaning
Respiratory syncytial virus (RSV) infection in early life is suspected to play a role in the development of postbronchiolitis wheezing and asthma. Reinfection is common at all ages, but factors that determine the development of altered airway function after reinfection are not well understood. This study was conducted in a mouse model to define the role of age in determining the consequences on airway function after reinfection. Mice were infected shortly after birth or at weaning and were reinfected 5 wk later, followed by assessment of airway function, airway inflammation, and lung histopathology. Infection of mice at weaning elicited a protective airway response upon reinfection. In this age group, reinfection resulted in increased airway inflammation, but without development of airway hyperresponsiveness (AHR) or eosinophilia and decreased IL-13 levels. By contrast, neonatal infection failed to protect the airways and resulted in enhanced AHR after reinfection. This secondary response was associated with the development of airway eosinophilia, increased IL-13 levels, and mucus hyperproduction. Both CD4- and CD8-positive T cells were a source of IL-13 in the lung, and inhibition of IL-13 abolished AHR and mucus production in these mice. Inoculation of UV-inactivated virus failed to elicit these divergent responses to reinfection, emphasizing the requirement for active lung infection during initial exposure. Thus, neonatal RSV infection predisposes to the development of airway eosinophilia and enhanced AHR via an IL-13-dependent mechanism during reinfection, whereas infection at a later age protects against the development of these altered airway responses after reinfection.
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1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Park, Jung Won(박중원) ORCID logo https://orcid.org/0000-0003-0249-8749
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