PT  - JOURNAL ARTICLE
AU  - K. Tsuji
AU  - S. Yamamoto
AU  - W. Ou
AU  - N. Nishi
AU  - I. Kobayashi
AU  - M. Zaitsu
AU  - E. Muro
AU  - Y. Sadakane
AU  - T. Ichimaru
AU  - Y. Hamasaki
TI  - dsRNA enhances eotaxin-3 production through interleukin-4 receptor upregulation in airway epithelial cells
AID  - 10.1183/09031936.05.00010805
DP  - 2005 Nov 01
TA  - European Respiratory Journal
PG  - 795--803
VI  - 26
IP  - 5
4099  - http://erj.ersjournals.com/content/26/5/795.short
4100  - http://erj.ersjournals.com/content/26/5/795.full
SO  - Eur Respir J2005 Nov 01; 26
AB  - The exacerbation of asthma during viral infections is mainly explained by neutrophils infiltrating into the airways. However, enhanced functions of eosinophils are also observed. The aim of this study was to reveal the mechanism of how eosinophils are activated during and after viral infection of the airways, using a model of viral infection. A synthetic double-stranded RNA, poly inosinic-cytidyric acid (poly(IC)), was transfected to a human airway epithelial cell line (BEAS-2B) and the primary bronchial epithelial cells, to mimic a viral infection. The production of chemokines from the cells was investigated. The transfection of poly(IC), alone, marginally affected the eotaxin-3 production of the cells. However, the transfection of poly(IC) prior to interleukin (IL)-4 stimulation enhanced eotaxin-3 production. Poly(IC) transfection increased mRNA and protein expressions of IL-4 receptor (R)α and IL-2Rγ, components of the IL-4R. In BEAS-2B cells, IL-4-mediated phosphorylation of signal transducer and activator of transcription six was enhanced in poly(IC) transfected cells. This was reversed by the addition of anti-IL-4Rα antibody, suggesting the role of an increased number of IL-4 receptors in enhanced IL-4-induced eotaxin-3 production. Poly(IC)-induced upregulation of IL-4Rα was inhibited by treatment with cycloheximide or dexamethasone. In conclusion, these results suggest that viral airway infection may enhance interleukin-4-induced eotaxin-3 production through upregulation of the interleukin-4 receptor in airway epithelial cells.