Egypt J Pediatr Allergy Immunol, (October 2019), Volume No. 17, Issue 02  
Egypt J Pediatr Allergy Immunol 2019 ; 17 ( 02 ) : 87 - 95
, ESP - 281  
Original articles
Can montelukast correct immune dysregulation in preschool children with mild persistent asthma?
Amany M. El-Kelany   Maha Anani   Hanan H. Omar   Asmaa A. Hashem   Enas Fathy    
Background: Asthma is the most common inflammatory disorder among preschool and school-age children. Regulation of immune cells and their cytokines is essential to control asthma. Montelukast is a leukotriene receptor antagonist that suppresses inflammatory cell proliferation, and reduces cytokines and mediator secretion. Objective: The research team's goal was to study the immunological parameters among mild asthmatic patients before and after the treatment with Montelukast . Methods: Forty preschool children with mild persistent asthma and twenty healthy, non-allergic children were included in the study. Blood eosinophil count, total IgE, serum IL-4, IL-10, and IL-13 levels were assessed. T helper (CD3+CD4+) and T regulatory (CD4+CD25+) cell counts were measured using flow cytometry; for mild asthmatics before and after six weeks of treatment with Montelukast and for the control group. Results: Asthmatic children have shown a significant elevation of serum levels of IgE, IL4 and IL13, and also an increase of eosinophils, total lymphocyte T cells and T helper cell count. However; serum levels of IL10 and Treg cell count was lower in asthmatics compared to control. Following six weeks of Montelukast treatment, all immunological parameters improved. There was a significant elevation of serum levels of IL10 and Treg cell count, with a decrease in serum levels of IgE, IL4 and IL13; eosinophil counts, and helper T cells. Conclusion: Montelukast treatment improves the impaired immunological balance of mild asthmatic children through the increase of serum IL-10, T regulatory cell counts that have anti-inflammatory and immunoregulatory effects. It also decreases T helper cells and their proinflammatory cytokines.