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

Baraldo S, Faffe DS, Moore PE, Whitehead T, McKenna M, Silverman ES, Panettieri RA, Shore SA
Am J Physiol Lung Cell Mol Physiol. 2003 284 (6): L1093-102

PMID: 12588703 · DOI:10.1152/ajplung.00300.2002

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 > or =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 micro M), 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 > or =10 ng/ml caused an approximately 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 PGE(2) 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.

MeSH Terms (19)

Cells, Cultured Chemokine CCL11 Chemokines, CC Cyclooxygenase 2 Dinoprostone Drug Synergism Gene Expression Humans Interleukin-8 Interleukin-9 Interleukin-13 Isoenzymes Membrane Proteins Mitogen-Activated Protein Kinases Muscle, Smooth Phosphorylation Prostaglandin-Endoperoxide Synthases Trachea Tumor Necrosis Factor-alpha

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