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Published ahead of print on October 12, 2006, doi:10.1165/rcmb.2006-0231OC

Am. J. Respir. Cell Mol. Biol., Volume 36, Number 3, March 2007, 324-332

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Submitted on June 27, 2006
Revised on October 6, 2006

IL-2 and IL-18 Attenuation of Airway Hyperresponsiveness Requires STAT4, Interferon-{gamma}, and NK Cells

Shigeki Matsubara1, Katsuyuki Takeda1, Taku Kodama1, Anthony Joetham1, Nobuaki Miyahara1, Toshiyuki Koya1, Christina H Swasey1, Masakazu Okamoto1, Azzeddine Dakhama1, and Erwin W Gelfand1*

1 Division of Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO, USA

* To whom correspondence should be addressed. E-mail: gelfande{at}njc.org.

Interleukin (IL)-18 is known to induce interferon (IFN)-{gamma} production, which is enhanced when combined with IL-2. In the present study, we investigated whether the combination of exogenous IL-2 and IL-18 alters airway hyperresponsiveness (AHR) and airway inflammation. Sensitized mice exposed to ovalbumin (OVA) challenge developed AHR, inflammatory cells in the bronchoalveolar lavage (BAL) fluid, and increases in levels of Th2 cytokines and goblet cell numbers. The combination of IL-2 and IL-18, but neither alone, prevented these change while increasing levels of IL-12 and IFN-{gamma}. The combination of IL-2 and IL-18 was ineffective in IFN-{gamma}-deficient and signal transducer and activator of transcription (STAT)4-deficient mice. Flow cytometry analysis showed significant increases in numbers of IFN-{gamma} positive natural killer (NK) cells in the lung after treatment with the combination therapy and transfer of lung NK cells isolated from sensitized and challenged mice treated with the combination significantly suppressed AHR and BAL eosinophilia. These data demonstrate that the combination of IL-2 and IL-18 prevents AHR and airway inflammation, likely through IL-12-mediated induction of IFN-{gamma} production in NK cells.




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[Abstract] [Full Text] [PDF]


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