Lymphocyte glucocorticoid receptors in asthmatic and control subjects

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Abstract
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. To better understand glucocorticoid pharmacology in asthmatics, glucocorticoid receptors were assayed by directly binding a radioactively labeled glucocorticoid hormone, dexamethasone, to intact lymphocytes prepared from the peripheral blood of [human] 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). The number of lymphocyte glucocorticoid receptors and the apparent affinity of dexamethasone for receptors are probably 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.