Stress and Neuroendocrine Regulation of Immune Responses

摘要

Administration of mice of stressors, such as electric footshock or restraint results in decreases of spleen and thymus weights, and in a variable decrease in mitogen-stimulated lymphocyte proliferation. This variability can be decreased with careful attention of time factors when processing the tissues form large numbers of animal. However, a large part of it probably reflects the prior immunological history of the animals. When the stressors are applied acutely, the stress-induced deficits in lymphocyte proliferation are prevented by prior adrenalectomy, suggesting the involvement of adrenal glucocorticoids. The deficits observed after chronic stress, can be prevented by chronic treatment with thymosin fraction 5. Administration to mice of supernatants from mitogen-stimulated rat spleen cells increases plasma corticosterone, but with little change in brain catecholamines. Parental administration of Newcastle disease virus (NDV) results in an activation of the pituitary-adrenal axis which requires an intact pituitary. Previous results that claimed these effects to be independent of the pituitary can be explained by incomplete hypophysectomy. The NDV administration also markedly depresses spleen cell proliferative responses. The increases in plasma corticosterone are paralleled by activation of certain brain neurotransmitter systems, notably the catecholamines. Concentrations of the norepinephrine metabolite MHPG and of tryptophan are increased in most brain regions, and dopamine and serotonin metabolites in a few. These changes resemble those observed with stressors such as footshock and restraint, suggesting that virus infection can be regarded as stressful. (SDW)