Kaneko H, Matsui E, Asano T, et al. Pediatr Allergy Immunol. 2006;17:370–375
PURPOSE OF THE STUDY. Several studies have suggested that respiratory syncytial virus (RSV) bronchiolitis induces a change in the cytokine-production profile in childhood. The authors of this study sought to determine if the RSV-induced cytokine production was affected by the patient's atopic background.
STUDY POPULATION. Fourteen children between 1 month and 14 years of age who were admitted to the hospital with RSV infection and divided into 2 groups: those who were nonatopic and those who were atopic.
METHODS. Interferon-γ (IFN-γ) and interleukin 4 (IL-4) in the supernatant of peripheral blood mononuclear cells was measured after culture for 24 hours in the presence of phytohemagglutinin, IL-12, or IL-18.
RESULTS. In RSV-infected infants with atopic diseases, IFN-γ production from IL-12–or especially IL-18–stimulated peripheral blood mononuclear cells was subtotally suppressed in the acute phase, whereas in RSV-infected infants without atopic diseases, IFN-γ production was not suppressed in the acute phase.
CONCLUSIONS. The IFN-γ suppression observed in the atopic group was not caused by the immaturity of the infants’ immune system, because reduced IFN-γ production to RSV was not observed in the infants in the nonatopic group. IFN-γ suppression in regard to RSV infection might be caused by some genetic factor involved in the development of atopic disease, such as IL-18 signal cascade.
REVIEWER COMMENTS. Several studies have suggested a link between RSV infection and the development of persistent wheezing later in childhood. However, a causal role for RSV infection in early life in the development of asthma is not clear. The results of this study indicate that there may be a genetic predisposition to T-helper 2–type immune responses to RSV in atopic children, which may play a role in the development of recurrent wheezing in this subset of children.
- Copyright © 2007 by the American Academy of Pediatrics