Volume 122, Issue 4 , Pages 726-733.e3, October 2008
Cytokine response after severe respiratory syncytial virus bronchiolitis in early life
Background
Immune response after viral infection usually involves TH1-mediated response; however, severe respiratory syncytial virus (RSV) infection appears to be associated with the development of asthma, a TH2-predominant phenotype.
Objective
To understand the early and subsequent immunologic response to a serious RSV infection in children over time.
Methods
A total of 206 previously healthy infants hospitalized with severe RSV bronchiolitis were enrolled in a prospective cohort called the RSV Bronchiolitis in Early Life study. Peripheral blood T cells were obtained immediately after RSV infection and at 2, 4, and 6 years of age, stimulated with phorbol 12-myristate 13-acetate and ionomycin, and analyzed for IL-2, IL-4, IL-13, and IFN-γ by flow cytometry and real-time PCR.
Results
Of the children, 48% (n = 97) developed asthma (physician-diagnosed), and 48% (n = 97) had eczema by age 6 years; 32% (n = 48 of 150) developed allergic sensitization by 3 years of age. Children with asthma had lower IL-13 expression at 6 years of age than those without (P = .001). IFN-γ, IL-2, and IL-4 levels did not differ by asthma or eczema status during follow-up (all P > .05). Allergic sensitization was not associated with differences in cytokine levels during follow-up (all P > .05).
Conclusion
Severe RSV infection early in life is associated with a high incidence of asthma and eczema. Contrary to expectations, subsequent immunologic development in those who developed asthma, eczema, or allergic sensitization was not associated with a TH2 phenotype in the peripheral blood.
Key words: RSV bronchiolitis, asthma, eczema, allergic sensitization, cytokines
Abbreviations used: FACS, Fluorescence-activated cell sorting, RBEL, RSV Bronchiolitis in Early Life study, RSV, Respiratory syncytial virus
Supported by National Institutes of Health grant no. HL 61895.
Disclosure of potential conflict of interest: The authors have declared that they have no conflict of interest.
PII: S0091-6749(08)01318-3
doi:10.1016/j.jaci.2008.07.010
© 2008 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Volume 122, Issue 4 , Pages 726-733.e3, October 2008
