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Am. J. Respir. Cell Mol. Biol., Volume 22, Number 6, June, 2000 649-656

Interleukin-9 Upregulates Mucus Expression in the Airways

Jamila Louahed, Masao Toda, Jin Jen, Qutayba Hamid, Jean-Cristophe Renauld, Roy C. Levitt, and Nicholas C. Nicolaides

Magainin Institute of Molecular Medicine, Magainin Pharmaceuticals, Inc., Plymouth Meeting, Pennsylvania; Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada; Johns Hopkins University, Medicine Department of Otolaryngology-Head and Neck Surgery and Oncology, Baltimore, Maryland; and Ludwig Institute for Cancer Research, Brussels Branch, and the Experimental Medicine Unit, University of Louvain, Brussels, Belgium

Interleukin (IL)-9 has recently been shown to play an important role in allergic disease because its expression is strongly associated with the degree of airway responsiveness and the asthmatic-like phenotype. IL-9 is a pleiotropic cytokine that is active on many cell types involved in the allergic immune response. Mucus hypersecretion is a clinical feature of chronic airway diseases; however, the mechanisms underlying the induction of mucin are poorly understood. In this report, we show that IL-9 regulates the expression of a subset of mucin genes in lung cells both in vivo and in vitro. In vivo, the constitutive expression of IL-9 in transgenic mice results in elevated MUC2 and MUC5AC gene expression in airway epithelial cells and periodic acid-Schiff-positive staining (reflecting mucous glycogenates). Similar results were observed in C57BL/6J mice after IL-9 intratracheal instillation. In contrast, instillation of the T helper 1-associated cytokine interferon gamma  failed to induce mucin production. In vitro, our studies showed that IL-9 also induces expression of MUC2 and MUC5AC in human primary lung cultures and in the human muccoepidermoid NCI-H292 cell line, indicating a direct effect of IL-9 on inducing mucin expression in these cells. Altogether, these results suggest that upregulation of mucin by IL-9 might contribute to the pathogenesis of human inflammatory airway disorders, such as asthma. These data extend the role of the biologic processes that IL-9 has on regulating the many clinical features of asthma and further supports the IL-9 pathway as a key mediator of the asthmatic response.




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