Background Cysteinyl leukotrienes are potent pro-inflammatory mediators that contribute to the pathophysiologic features observed in allergic asthma. Inhibitors of leukotriene receptors represent novel therapy in asthma treatment. In addition to the protection from early asthmatic responses, these drugs have recently been shown to protect from late airway responses too.
Methods We studied the effect of treatment with an oral antagonist of cysteinyl leukotriene receptors on the increased expression of the low-affinity IgE receptor, CD23, on B cells, and of its ligands, CD11b and CD11c, on CD4+ T cells and monocytes in peripheral blood of patients with allergic asthma. In this uncontrolled open-label study, 14 children with allergic asthma received montelukast, a cysteinyl leukotrine receptor antagonist, for a period of 6 weeks after demonstrating forced expiratory volume in 1 s (FEV1) of less than 80% of the predicted value. Samples of peripheral heparinized blood and sera were obtained before and after therapy completion. Three-colour immunofluorescence analysis was performed, and expression of CD11b and CD11c on CD4+ T lymphocytes and monocytes as well as the expression of CD21 and CD23 on B cells were determined (n=12). Peripheral blood eosinophil count, changes in FEV1 and peak expiratory flow rate (PEFR), asthma exacerbations, and as-needed use of β-agonist were also monitored.
Results Montelukast improved FEV1 and PEFR, and decreased peripheral eosinophil counts in all study patients. There was no significant change in the expression of CD21 and CD23 on B cells. The expression of CD11c on CD4+ T cells and of both CD11b and CD11c on monocytes remained similar to the pretreatment expression. However, the percentage of CD11b+CD4+ T lymphocytes significantly decreased after treatment with montelukast. This was accompanied by a significant decrease in the levels of total IgE.
Conclusion The capacity of 6-week montelukast therapy to reduce the percentage of CD11b CD4+ T cells might be a mechanism leading to the immune response modulation on this T cell subset interaction with CD23-expressing B cells and subsequent down-regulation of IgE synthesis.
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