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This Article Full Text Full Text (PDF) All Versions of this Article: 290/6/L1238    most recent 00301.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Lajoie-Kadoch, S. Articles by Hamid, Q. Search for Related Content PubMed PubMed Citation Articles by Lajoie-Kadoch, S. Articles by Hamid, Q.

TNF- and IFN- inversely modulate expression of the IL-17E receptor in airway smooth muscle cells

¹Meakins-Christie Laboratories, McGill University, Montréal, Québec; and Departments of ²Physiology and ³Immunology, University of Manitoba, Winnipeg, Manitoba, Canada

Submitted 13 July 2005 ; accepted in final form 13 January 2006

The interleukin-17B receptor (IL-17BR) is expressed in a variety of tissues and is upregulated under inflammatory conditions. This receptor binds both its cognate ligand IL-17B and IL-17E/IL-25, a novel cytokine known to promote Th2 responses. The present study shows that airway smooth muscle cells express IL-17BR in vitro and that its expression is upregulated by TNF- and downregulated by IFN-. Our data indicate that TNF- upregulates IL-17BR mainly through nuclear factor-B as assessed with the IB kinase 2 inhibitor AS-602868. In addition, both IFN- and dexamethasone are able to antagonize a TNF--induced IL-17BR increase in mRNA expression. The mitogen-activated protein kinase kinase inhibitor U0126 totally reversed the inhibition observed with IFN-, suggesting the involvement of the extracellular signal-regulated kinase pathway in this effect. In addition, on stimulation with IL-17E, airway smooth muscle cells increase their expression of ECM components, namely procollagen-I and lumican mRNA. Furthermore, immunohistochemical analysis of biopsies from asthmatic subjects reveals that this receptor is abundant in smooth muscle layers. This is the first report showing IL-17BR receptor in structural cells of the airways. Our results suggest a potential proremodeling effect of IL-17E on airway smooth muscle cells through the induction of ECM and that its receptor is upregulated by proinflammatory conditions.

human; stromal cells; cytokine receptors; cytokines; extracellular matrix; tumor necrosis factor-; interferon-; interleukin-17E

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