IL-9 induces chemokine expression in lung epithelial cells and baseline airway eosinophilia in transgenic mice
✍ Scribed by Qu Dong; Jamila Louahed; Anne Vink; Christine D. Sullivan; Carol J. Messler; Yuhong Zhou; Angela Haczku; Francois Huaux; Mohamed Arras; Kenneth J. Holroyd; Jean-Christophe Renauld; Roy C. Levitt; Nicholas C. Nicolaides
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 145 KB
- Volume
- 29
- Category
- Article
- ISSN
- 0014-2980
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✦ Synopsis
Recent data have identified IL-9 as a key cytokine in determining susceptibility to asthma. These data are supported by the finding that allergen-exposed IL-9-transgenic mice exhibit many features that are characteristic of human asthma (airway eosinophilia, elevated serum IgE and bronchial hyperresponsiveness) as compared to the background strain. A striking feature of these animals is a robust peribronchial and perivascular eosinophilia after allergen challenge, suggesting that IL-9 is a potent factor in regulating this process. In an attempt to gain insights into the molecular mechanism governing IL-9 modulation of lung eosinophilia, we investigated the ability of this cytokine to induce the expression of CC-type chemokines in the lung because of their effect on stimulating eosinophil chemotaxis. Here we show that IL-9-transgenic mice in contrast to their congenic controls exhibit baseline lung eosinophilia that is associated with the up-regulation of CC-chemokine expression in the airway. This effect appears to be through a direct action of IL-9 because the addition of recombinant IL-9 to primary epithelial cultures and cell lines induced the expression of these chemokines in vitro. These data support a mechanism for IL-9 in regulating the expression of eosinophil chemotactic factors in lung epithelial cells.