Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 404, Issue 4, Pages 922-927Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2010.12.082
Keywords
Bronchial epithelial cells; Alveolar macrophages; dsRNA; IL-13; IFN-lambda
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Funding
- Ministry of Education, Science, and Culture of Japan
- National Institute of Biomedical Innovation, Japan
- Grants-in-Aid for Scientific Research [22390167] Funding Source: KAKEN
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Acute asthma exacerbations are frequently associated with respiratory viral infections. Although impaired production of type III IFNs (IFN-lambda s) is related to the severity of asthma exacerbation, the mechanisms underlying deficient IFN-lambda production in asthma are poorly understood. Airway epithelial cells were stimulated in vitro with a synthetic mimetic of viral double-stranded RNA (dsRNA). IL-13, a crucial cytokine responsible for asthma pathogenesis, suppressed dsRNA-induced expression of IFN-lambda s, and JAK inhibitor AG490 prevented the suppression by IL-13. IL-13 per se did not affect IFN-lambda production or the expressions of membrane dsRNA receptor TLR3 and of cytoplasmic receptors RIG-I and MDA5. IL-13-deficient mice exhibited more enhanced IFN-lambda expression after intratracheal instillation of dsRNA than wildtype mice, whereas IFN-lambda expression after dsRNA was absent in the mouse lungs of the OVA-induced asthma model. These findings suggest that IL-13 may be a putative cytokine suppressing IFN-lambda production against airway viral infections in asthmatics. (C) 2010 Elsevier Inc. All rights reserved.
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