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Interleukin-13 Alters Mucociliary Differentiation of Human Nasal Epithelial Cells*

Marie Skowron, PhD(c); Eric Perret, PhD; Francelyne Marano, PhD; Daniel Caput, PhD; Frédéric Tournier, PhD
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*From the Laboratoire de Cytophysiologie et Toxicologie Cellulaire (Drs. Skowron, Tournier, and Marano), Université Paris, Paris, France; and Sanofi-Synthelabo Recherche (Drs. Perret and Caput), Labège, France.

Correspondence to: Frédéric Tournier, PhD, Laboratoire de Cytophysiologie et Toxicologie Cellulaire, Case 7073, Tour 53-54, 3ème Étage, 2, Place Jussieu, 75251 Paris Cedex 05, France; e-mail: f-tournier@paris7.jussieu.fr



Chest. 2003;123(3_suppl):373S-374S. doi:10.1378/chest.123.3_suppl.373S
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Lesions of the airway epithelium are frequently observed in asthma patients. Therefore, inflammatory mediators such as chemokines or cytokines may influence airway remodeling. Among these cytokines, interleukin (IL)-13 recently has emerged as a pivotal molecule with which to promote airway hyperresponsiveness.1 We have investigated the effect of IL-13 on the mucociliary differentiation of human nasal epithelial cells in primary culture. IL-13 alters ciliated cell differentiation and, in parallel, largely increases the proportion of secretory cells in a dose-dependent and time-dependent manner, and impairs lateral cell contacts. Treatment with IL-13 and increasing amounts of an IL-4 mutant (Y124D), which is a selective antagonist of the IL-4/IL-13 shared receptor, abolishes the effects of IL-13.2 Using differential screening of treated and nontreated epithelial cells during differentiation, we showed that transforming growth factor-β1 gene expression is increased in the presence of the cytokine, reinforcing the idea that IL-13 could induce tissue fibrosis by selectively activating transforming growth factor-β1, as was recently shown in mice.3 Because multiple IL-13 effects contribute to the asthma phenotype, inhibiting the cytokine or its receptors in vivo may be relevant in patients with chronic lung diseases such as asthma.

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