Abstract
The exacerbation of asthma during viral infections is mainly explained by neutrophils infiltrating into 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. Eotaxin-3 is a chemokine that shows potent chemoattractant activity toward eosinophils. Airway epithelial cells produced eotaxin-3 after stimulation with the Th2 cytokine interleukin (IL) -4. When the cells were cultured with Th1 cytokine interferon (IFN) -γ and IL-4 simultaneously, IFN-γ inhibited the production of IL-4-induced eotaxin3. On the other hand, pretreatment of the cells with IFN-γ dose-dependently enhanced IL-4-induced eotaxin-3 production. IFN-γ also increased expression of IL-4 receptors in a time- and a dose-dependent manner. AS a model of viral infedction, a synthetic double-strand RNA, poly inosinic-cytidynic acid ( Poly (IC)), was transfected to the airway epithelial cells. Also poly (IC) transfecion increased expression of IL-4R, and pretreatment of the cells with poly (IC) enhanced IL-4-induced eotaxin-3. These results suggest that viral airway infection may enhance IL-4-induced eotaxin-3 production through upregulation of the IL-4R in airway epithelial cells. Thus, mediators that exist in the airway might modulate production of chemokines by affecting the expression of several molecules such as cytokine receptors of airway epithelial cells.
