Beta2-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. Beta2-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 beta-adrenoceptors occurs in long-term beta2-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 beta2-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 beta2-agonist exposure predisposed differentiation of T lymphocytes towards Th2 while that of Th1 was relatively suppressed, especially in cord blood T cells. Hence, beta2-agonists, despite their effect in symptomatic rescue in asthma, should not be used indiscriminately as long-term therapeutic agents.