期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 284, 期 6, 页码 L1093-L1102出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00300.2002
关键词
eotaxin; interleukin-8; tumor necrosis factor-alpha; interleukin-1 beta; cyclooxygenase-2; interleukin-13; human airway smooth muscle cells; extracellular signal-regulated protein kinase
资金
- NHLBI NIH HHS [HL-04395, R01 HL064063, HL-67664, HL-55301, HL-64063, R01 HL055301, K08 HL004395, HL-67663, HL-56383] Funding Source: Medline
- NIEHS NIH HHS [ES-00002] Funding Source: Medline
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 greater than or equal to30 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 muM), 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 greater than or equal to10 ng/ml caused an similar to50% 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.
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