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Am J Physiol Lung Cell Mol Physiol 284: L1093-L1102, 2003. First published February 14, 2003; doi:10.1152/ajplung.00300.2002
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Vol. 284, Issue 6, L1093-L1102, June 2003

Interleukin-9 influences chemokine release in airway smooth muscle: role of ERK

Simonetta Baraldo, Deborah S. Faffe, Paul E. Moore, Timothy Whitehead, Matthew McKenna, Eric S. Silverman, Reynold A. Panettieri Jr., and Stephanie A. Shore

Physiology Program, Harvard School of Public Health, Boston, Massachusetts 02115; and Pulmonary and Critical Care Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104

Interleukin (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, 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 time-dependent fashion, and U-0126 (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 caused an ~50% increase in release of eotaxin evoked by IL-13 (10 ng/ml). U-0126 blocked the synergism between IL-9 and IL-13 on eotaxin release. IL-9 had no effect on cyclooxygenase-2 (COX-2) expression or PGE2 release and did not augment the COX-2 expression that was induced by IL-1beta . 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.

eotaxin; interleukin-8; tumor necrosis factor-alpha ; interleukin-1beta ; cyclooxygenase-2; interleukin-13; human airway smooth muscle cells; extracellular signal-regulated protein kinase


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