Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 130, Issue 5, Pages 1187-+Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2012.07.031
Keywords
TSLP; RSV; asthma; epithelium; T(H)2
Categories
Funding
- National Institutes of Health [AI068731, HL098067, AR055695, AR056113, HL102708, AI060389, AI083019, HL059178]
- National Institutes of Health (NIH)
- NIH
- American Academy of Allergy, Asthma Immunology
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Background: Respiratory viral infection, including respiratory syncytial virus (RSV) and rhinovirus, has been linked to respiratory disease in pediatric patients, including severe acute bronchiolitis and asthma exacerbation. Objective: The study examined the role of the epithelial-derived cytokine thymic stromal lymphopoietin (TSLP) in the response to RSV infection. Methods: Infection of human airway epithelial cells was used to examine TSLP induction after RSV infection. Air-liquid interface cultures from healthy children and children with asthma were also tested for TSLP production after infection. Finally, a mouse model was used to directly test the role of TSLP signaling in the response to RSV infection. Results: Infection of airway epithelial cells with RSV led to the production of TSLP via activation of an innate signaling pathway that involved retinoic acid induced gene I, interferon promoter-stimulating factor 1, and nuclear factor-kappa B. Consistent with this observation, airway epithelial cells from asthmatic children a produced significantly greater levels of TSLP after RSV infection than cells from healthy children. In mouse models, RSV-induced TSLP expression was found to be critical for the development of immunopathology. Conclusion: These findings suggest that RSV can use an innate antiviral signaling pathway to drive a potentially nonproductive immune response and has important implications for the role of TSLP in viral immune responses in general. (J Allergy Clin Immunol 2012;130:1187-96.)
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