Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Skowron, M.
Right arrow Articles by Tournier, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Skowron, M.
Right arrow Articles by Tournier, F.
(Chest. 2003;123:373S-374S.)
© 2003 American College of Chest Physicians

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

Marie Skowron, PhD(c); Eric Perret, PhD; Francelyne Marano, PhD; Daniel Caput, PhD and Frédéric Tournier, PhD

* 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{at}paris7.jussieu.fr

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-ß1 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-ß1, 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.


    References
 TOP
 References
 

  1. Corry, DB (1999) IL-13 in allergy: home at last. Curr Opin Immunol 11,610-614[CrossRef][Medline]
  2. Laoukili, J, Perret, E, Willems, T, et al IL-13 alters mucociliary differentiation and ciliary beating of human respiratory epithelial cells. J Clin Invest 2001;108,1817-1824[CrossRef][ISI][Medline]
  3. Lee, CG, Homer, RJ, Zhu, Z, et al Interleukin-13 induces tissue fibrosis by selectively stimulating and activating transforming growth factor ß1. J Exp Med 2001;194,809-821[Abstract/Free Full Text]




This Article
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Skowron, M.
Right arrow Articles by Tournier, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Skowron, M.
Right arrow Articles by Tournier, F.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS