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Am J Physiol Lung Cell Mol Physiol (January 20, 2006). doi:10.1152/ajplung.00301.2005
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Submitted on July 13, 2005
Accepted on January 13, 2006

TNF{alpha} and IFN{gamma} inversely modulate expression of the IL-17E receptor in Airway Smooth Muscle Cells

Stephane Lajoie-Kadoch1, Philippe Joubert1, Severine Letuve1, Andrew J Halayko2, James G Martin1, Abdellilah Soussi-Gounni3, and Qutayba Hamid1*

1 Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada
2 Departement of Physiology, University of Manitoba, Winnipeg, Manitoba, Canada
3 Departement of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada

* To whom correspondence should be addressed. E-mail: qutayba.hamid{at}mcgill.ca.

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 illustrates that airway smooth muscle cells express IL-17BR in vitro and that its expression is upregulated by TNF{alpha} and downregulated by IFN{gamma}. Our data indicates that TNF{alpha} upregulates IL-17BR mainly through NF-{kappa}B as assessed with the IKK2 inhibitor, AS602868. In addition, both IFN{gamma} and dexamethasone are able to antagonize a TNF{alpha}-induced IL-17BR increase in mRNA expression. The MEK inhibitor, U0126, totally reversed the inhibition observed with IFN{gamma}, suggesting the involvement of the ERK pathway in this effect. In addition, upon stimulation with IL-17E, ASMC increase their expression of extracellular matrix components, namely pro-collagen {alpha}1 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 pro-remodelling effect of IL-17E on airway smooth muscle cells through the induction of extracellular matrix and that its receptor is upregulated by proinflammatory conditions.




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