β2-agonist exerts differential effects on the development of cord blood T cells but not on peripheral blood T cells

Abstract

Asthma is a chronic inflammatory disease characterized by reversible airway obstruction caused by edematous airway lining, thickened mucosal secretions, and smooth muscle constriction. β2-adrenoceptor agonists are widely used in the treatment of bronchial asthma because of their ability to induce relaxation of airway smooth muscle. Evidence indicates that desensitization and down-regulation of β-adrenoceptors occurs in long-term β2-agonist therapy; and these medications were thought to cause increased severity of, and mortality in, asthma. The purpose of this study was to delineate further the potential adverse effects of β2-agonists on the development of T lymphocytes. T cells isolated from umbilical cord blood and adult peripheral blood were cultured in the presence of salbutamol. Intracellular staining with fluorescence-labeled antibodies was used to differentiate the frequency of type 1 T-helper (Th1) and type 2 T-helper (Th2) cells. The results showed a statistically significant inverse relationship between the concentration of salbutamol and the ratio of Th1 over Th2 on cord blood T cells. However, this trend was not observed in adult peripheral blood T cells. The data revealed another potential adverse effect in which chronic β2-agonist exposure predisposed differentiation of T lymphocytes towards Th2 while that of Th 1 was relatively suppressed, especially in cord blood T cells. Hence, β2-agonists, despite their effect in symptomatic rescue in asthma, should not be used indiscriminately as long-term therapeutic agents.