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Dong, Q. et al.

IL-9 induces chemokine expression in lung epithelial cells and baseline airway eosinophilia in transgenic mice.

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.[1]

References

IL-9 induces chemokine expression in lung epithelial cells and baseline airway eosinophilia in transgenic mice. Dong, Q., Louahed, J., Vink, A., Sullivan, C.D., Messler, C.J., Zhou, Y., Haczku, A., Huaux, F., Arras, M., Holroyd, K.J., Renauld, J.C., Levitt, R.C., Nicolaides, N.C. Eur. J. Immunol. (1999) [Pubmed]

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