Association of glucocorticoid with stress-induced modulation of body temperature, blood glucose and innate immunity.

To know the details of the mechanism on stress-associated responses, attention was first focused on body temperature and blood glucose after stress. Mice were exposed to restraint stress for 6 h. Under this condition, hypothermia (39 degrees C --> 33 degrees C) and hyperglycemia (150 mg/dl --> 350 mg/dl) were induced. Reflecting a stress-associated response, an increase of serum corticosterone (200 ng/ml --> up to 600 ng/ml) was observed. It was examined whether an administration of glucocorticoid induced a similar response. An injection of hydrocortisone (5.0 and 10.0 mg/mouse) simultaneously induced hypothermia and hyperglycemia. The effect on immunoparameters by an injection of hydrocortisone was examined. Although immunosuppression was seen as thymic atrophy and a decrease in the proportion of B cells in the liver, extrathymic T cells and NKT cells were found to be stress-resistant lymphocyte populations, especially in the liver. HSP70 mRNA was indicated to increase in the adrenal glands in response to the hydrocortisone injection. All these responses, including hypothermia, hyperglycemia and immunomodulation, induced by the hydrocortisone injection were suppressed by pre-administration of a glucocorticoid receptor antagonist (RU-486). These results suggest that glucocorticoid is one of the important mediators of the stress-associated responses.