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Am J Physiol Lung Cell Mol Physiol (February 14, 2003). doi:10.1152/ajplung.00300.2002
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Submitted on September 4, 2002
Accepted on February 6, 2003

INTERLEUKIN-9 INFLUENCES CHEMOKINE RELEASE IN AIRWAY SMOOTH MUSCLE: ROLE OF ERK

Simonetta Baraldo1, Deborah S. Faffe1, Paul E. Moore1, Timothy Whitehead1, Matthew McKenna1, Eric S. Silverman1, Reynold A. Panettieri Jr.2, and Stephanie A. Shore1*

1 Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA
2 Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA

* To whom correspondence should be addressed. E-mail: sshore{at}hsph.harvard.edu.

Interleukin-9 (IL-9) is a pleiotropic cytokine that has been proposed as a candidate gene for asthma. As IL-9 expression is correlated with airway hyperresponsiveness in animals, we examined the effects of IL-9 on cultured human airway smooth muscle (HASM) cells. IL-9 alone had no effect on IL-8 release, but at concentrations of 30 ng/ml and higher, IL-9 significantly increased IL-8 release induced by TNF{alpha}. IL-9 increased phosphorylation of extracellular signal-regulated protein kinase (ERK, p42 and p44) in a concentration- and timedependent fashion and U0126 (10 µM), which inhibits ERK phosphorylation, abolished the synergism between TNF{alpha} and IL-9 on IL-8 release. IL-9 alone had no effect on eotaxin release into HASM cell supernatants, but at concentrations of 10 ng/ml and higher, caused an approximate 50% increase in release of eotaxin evoked by IL-13 (10 ng/ml). U0126 blocked the synergism between IL-9 and IL-13 on eotaxin release. IL-9 had no effect on COX-2 expression or PGE2 release, and did not augment the COX-2 expression that was induced by IL-1{beta}. Our results indicate that airway smooth muscle is a target for IL-9 and that IL-9 amplifies the potential for these cells to recruit eosinophils and neutrophils into the airways by a mechanism involving ERK.




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