Effect of montelukast on the expression of CD4+CD25+ regulatory T cells in children with acute bronchial asthma

摘要

The aim of this study was to investigate the effect of montelukast on the expression of CD4⁺CD25⁺ regulatory T cells in children with acute bronchial asthma. Fifty-six child patients with acute bronchial asthma treated in the Department of Pneumology at the Shangluo Central Hospital were selected and randomly divided into the control group (n=28) and treatment group (n=28). The control group was treated with the conventional therapy of bronchial asthma, while the treatment group received montelukast on the basis of the control group for 7 days. The clinical symptoms, lung function and proportion of CD4⁺CD25⁺ regulatory T cells in peripheral T lymphocyte subsets in patients in the two groups were observed. Moreover, the levels of inflammatory factors and immunoglobulin E (IgE) in peripheral blood in both groups were detected. The effective treatment rate in the treatment group was significantly higher than that in the control group (P<0.05), and the forced expiratory volume in 1 sec/forced vital capacity (FEV1/FVC), peak expiratory flow (PEF) and 25% peak expiratory flow (PEF25) in the treatment group were significantly higher than those in the control group (P<0.05). The proportions of CD4⁺CD25⁺ regulatory T cells in the two groups after drug therapy were significantly increased. The proportion and content per unit volume of peripheral CD4⁺CD25⁺ regulatory T cells in the treatment group were obviously higher than those in the control group (P<0.01). After treatment, the levels of interleukin-4 (IL-4), IL-5 and IL-6 in peripheral blood in the two groups were significantly decreased. However, the levels of transferrin-γ (TFN-γ) and IL-10 were significantly increased (P<0.01). The IgE level in the treatment group was also significantly higher than that in the control group (P<0.01). In conclusion, montelukast can regulate the T helper 1 (Th1)/Th2 balance, increase the expression of CD4⁺CD25⁺ regulatory T cells, and improve the airway inflammation caused by acute bronchial asthma and the clinical symptoms and lung function of patients with acute bronchial asthma.