Lymphocyte glucocorticoid receptors in asthmatic and control subjects

Glucocorticoid hormones, which are widely used in the treatment of asthma, have been shown to potentiate physiological and biochemical beta-adrenergic responsiveness in asthmatics. These effects are presumably mediated through glucocorticoid receptors. In order to better understand glucocorticoid pharmacology in asthmatics, we assayed glucocorticoid receptors by directly binding a radioactively labelled glucocorticoid hormone, dexamethasone, to intact lymphocytes prepared from the peripheral blood of asthmatics and control subjects. Binding studies were performed with dexamethasone at 100 nM and 5 nM concentrations. At 100 nM dexamethasone, the mean number of lymphocyte glucocorticoid receptors (per cell) in control subjects (7191 ± 385, n = 9) was not significantly different from that in asthmatic subjects (7772 ± 437, n =9). At 5 nM dexamethasone, the mean number of glucocorticoid receptors in control subjects (1177 ± 194, n=5) was not significantly different from that in asthmatic subjects (1215 ± 108, n=8). At 100 nM dexamethasone, males had significantly more receptors (7939 ± 360, n=11) than females (6764 ± 72, n=7). Our results suggest that the number of lymphocyte glucocorticoid receptors and the apparent affinity of dexamethasone for receptors are not related to the presence or severity of asthma; however, a significant sex effect exists which should be corrected for in future studies of lymphocyte glucocorticoid receptors.