TY - JOUR
T1 - Lymphocyte glucocorticoid receptors in asthmatic and control subjects
AU - Tsai, B. S.
AU - Watt, G.
AU - Koesnadi, K.
AU - Townley, R. G.
PY - 1984
Y1 - 1984
N2 - 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.
AB - 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.
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U2 - 10.1111/j.1365-2222.1984.tb02217.x
DO - 10.1111/j.1365-2222.1984.tb02217.x
M3 - Article
C2 - 6467559
VL - 14
SP - 363
EP - 371
JO - Clinical Allergy
JF - Clinical Allergy
SN - 0954-7894
IS - 4
ER -