The effect of montelukast on soluble interleukin-2 receptor and tumor necrosis factor α in pediatric asthma
Proinflammatory cytokines such as tumor necrosis factor (TNF) α and soluble interleukin 2 receptor (sIL-2R) are very important mediators in induction of inflammatory response in lung. The aim of this study was to investigate anti-inflammatory response of cysteinyl leukotriene receptor antagonist montelukast on macrophage and T-cell activation by sIL-2R and TNF-α in mild atopic asthmatic children. Fifteen children with mild-to-moderate atopic asthma and 15 nonatopic children as control, enrolled in the study. Asthmatic children were treated with montelukast, 5-mg tablets, for 1 month. Lung function test forced expiratory volume in 1 second (FEV1) was performed before and after treatment. Serum TNF-α, sIL-2R, and eosinophil cationic protein levels were determined in the control group and in asthmatic children before and after treatment. The mean eosinophil cationic protein value was significantly decreased (33.1 ± 14.8 and 22.2 ± 12.1; p < 0.05) and FEV1 was significantly increased (86.9 ± 20.9 and 102.1 ± 12.7; p < 0.05) after 1 month treatment with montelukast. The mean serum IL-2R levels were significantly higher in the before treatment group than in the after treatment group (1061.9 ± 491 and 794 ± 230.9; p < 0.05) or in control subjects (581.1 ± 123; p < 0.01). The mean serum TNF-α level was higher in the before treatment group than in the after treatment group and control group (7.30 ± 3.93, 5.20 ± 1.46, and 4.95 ± 1.27; p < 0.05). There was a significant correlation between TNF-α and sIL-2R in patients before montelukast treatment (r = 0.674; p < 0.01). This study indicates that montelukast improves clinical parameters and shows anti-inflammatory response by decreasing serum sIL-2R and TNF-αlevels.
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Document Type: Research Article
Publication date: July 1, 2006
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