Role of α-adrenergic stimulus in stress-induced modulation of body temperature, blood glucose and innate immunity

Mice were exposed to restraint stress for 3 h. During this period, low body temperature (hypothermia, 39 °C → less than 37 °C) and high blood glucose levels (hyperglycemia, 150 mg/dl → up to 220 mg/dl) were simultaneously induced. Reflecting a stress-induced phenomenon, blood levels of catecholamines increased at that time. Administration of adrenaline (α-stimulus), but neither noradrenaline (α but less than adrenaline) nor isoproterenol (β), induced a similar stress-induced pattern of body temperature and blood glucose variations. This α-adrenergic effect was confirmed using α- and β-blockers in adrenaline-induced hypothermia and hyperglycemia. By applying this α-stimulus, the effect on immunoparameters was then investigated. Stress-resistant lymphocyte populations were found to be NK cells, extrathymic T cells and NKT cells, especially in the liver. Functional assays showed that both NK-cell cytotoxicity and NKT-cell cytotoxicity were augmented by α-stimulus. These results suggest that α-stimulus is one of the important factors in the stress-induced phenomenon and that it eventually produces hypothermia, hyperglycemia and innate-immunity activation seen during stress.