Interleukin-9 influences chemokine release in airway smooth muscle: role of ERK
| Autor: | Paul E. Moore, Reynold A. Panettieri, Simonetta Baraldo, Deborah S. Faffe, Timothy A. Whitehead, Matthew D. McKenna, Eric S. Silverman, Stephanie A. Shore |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Chemokine CCL11
Pulmonary and Respiratory Medicine MAPK/ERK pathway Eotaxin Chemokine Physiology medicine.medical_treatment Gene Expression Biology Dinoprostone Physiology (medical) medicine Humans Interleukin 9 Interleukin 8 Phosphorylation Cells Cultured Interleukin-13 Tumor Necrosis Factor-alpha Interleukin-8 Interleukin-9 Membrane Proteins Interleukin Drug Synergism Muscle Smooth Cell Biology Isoenzymes Trachea Cytokine Cyclooxygenase 2 Prostaglandin-Endoperoxide Synthases Chemokines CC Interleukin 13 Immunology biology.protein Mitogen-Activated Protein Kinases |
| Zdroj: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 284:L1093-L1102 |
| ISSN: | 1522-1504 1040-0605 |
| DOI: | 10.1152/ajplung.00300.2002 |
| Popis: | 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-α. 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-α 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 PGE2release and did not augment the COX-2 expression that was induced by IL-1β. 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. |
| Databáze: | OpenAIRE |
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