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Published ahead of print on July 1, 2004, doi:10.1165/rcmb.2004-0128OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 4, October 2004, 456-462

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Submitted on April 22, 2004
Revised on June 29, 2004

Upregulation of IL-4R by IFN-{gamma}; enhanced IL-4-induced eotaxin-3 production in airway epithelium

Shuichi Yamamoto1*, Ikuko Kobayashi1, Kohsuke Tsuji1, Natsuko Nishi1, Eriko Muro1, Michiko Miyazaki1, Masafumi Zaitsu1, Shigeyasu Inada1, Tomohiro Ichimaru1, and Yuhei Hamasaki1

1 Department of Pediatrics, Saga University, School of Medicine, Saga, Saga, Japan

* To whom correspondence should be addressed. E-mail: yamamot6{at}med.saga-u.ac.jp.

Airway epithelial cells produce a number of chemokines, including eotaxins. Among the three known eotaxins, Th2 cytokines have been observed to induce the expression of eotaxin-3 mRNA. This study investigated the effect of IFN-{gamma}, a Th1 cytokine, on Th2 cytokine-induced eotaxin-3 production in a bronchial epithelial cell line (BEAS-2B). BEAS-2B cells produced eotaxin-3 following stimulation with the Th2 cytokines IL-13 and IL-4. When BEAS-2B cells were cultured with varying concentrations of IFN-{gamma} for 24 hours, dose-dependent inhibition of Th2 cytokine-induced eotaxin-3 mRNA expression and protein production was observed. This was associated with down-regulation of STAT6 activation. On the other hand, two-day pre-treatment of BEAS-2B cells with IFN-{gamma} dose-dependently enhanced Th2 cytokine-induced eotaxin-3 mRNA expression and production. IFN-{gamma} also increased the mRNA expression and protein production of IL-4R{alpha} in a time- and dose- dependent manner. In addition, IL-2R{gamma}, a component of the type 1 IL-4R, was also upregulated by IFN-{gamma}. These results indicate that IFN-{gamma} has opposite effects on Th2 cytokine-induced eotaxin-3 production in BEAS-2B cells, depending on the length of exposure. Because high levels of IFN-{gamma} are produced during viral infection, airway viral infection may affect allergic airway inflammation in vivo by modulation of eotaxin-3 production.




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