The effect of montelukast on soluble interleukin-2 receptor and tumor necrosis factor alpha in pediatric asthma.
Proinflammatory cytokines such as tumor necrosis factor (TNF) alpha 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-alpha 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-alpha, 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-alpha 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-alpha 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-alpha levels.
Can
Murat
M
Department of Biochemistry, Karaelmas University of Medicine, Zonguldak, Turkey. drcanmurat@yahoo.com
Yüksel
Birol
B
Demirtaş
Selda
S
Tomaç
Nazan
N
D000085:Acetates / Q000627:therapeutic use*; D001249:Asthma / Q000097:blood* / Q000188:drug therapy*; D002648:Child; D003521:Cyclopropanes; D047150:Eosinophil Cationic Protein / Q000097:blood; D005260:Female; D006801:Humans; D020024:Leukotriene Antagonists / Q000627:therapeutic use*; D008297:Male; D011804:Quinolines / Q000627:therapeutic use*; D015375:Receptors, Interleukin-2 / Q000097:blood*; D012129:Respiratory Function Tests; D013440:Sulfides; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D000085:Acetates; D003521:Cyclopropanes; D020024:Leukotriene Antagonists; D011804:Quinolines; D015375:Receptors, Interleukin-2; D013440:Sulfides; D014409:Tumor Necrosis Factor-alpha; D047150:Eosinophil Cationic Protein; C479220:RNASE3 protein, human; C093875:montelukast