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Hormonal regulation of the immune response. II. Influence of pituitary and adrenal activity on immune responsiveness in vitro
Authors:R H Gisler  L Schenkel-Hulliger
Affiliation:1. Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, United States;2. Department of Psychology, The Ohio State University, United States;3. Department of Psychiatry and Behavioral Health, The Ohio State University College of Medicine, United States;1. Department of Psychology, UCLA, Los Angeles, CA, USA;2. Department of Psychiatry and Biobehavioral Sciences, UCLA, Los Angeles, CA, USA;3. Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, UCLA, Los Angeles, CA, USA;4. Department of Psychological Science, UCI, Irvine, CA, USA;1. Stress Research Institute, Department of Psychology, Stockholm University, SE-106 91, Stockholm, Sweden;2. Division of Psychology, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden;3. Osher Center for Integrative Medicine, ME Neuroradiologi, Karolinska Universitetssjukhuset, Stockholm, Sweden
Abstract:Exposure of mice to acceleration stress, ether anesthesia or injection of adrenocorticotropic hormone (ACTH) resulted in a transitory increase of plasma corticosterone concentrations. Spleen cells explanted at the moment of increased levels of corticosteroids reacted poorly to antigen in vitro. Adrenalectomy of the cell donors did not affect the immune reactivity of spleen cell cultures, nor did ACTH show any effect in adrenalectomized mice. On the other hand, hypophysectomy of the cell donors led to a persistent depression of the immune response. Treatment of hypophysectomized animals with somatotropic hormone (STH) prior to cell culture resulted in an almost normal immune capacity. Moreover, subsequent ACTH treatment no longer impaired immune reactivity, although it effectively increased plasma corticosterone levels. It is concluded that recovery from corticosteroid-induced depression of immune reactivity is accelerated in the presence of somatotropic hormone. In hypophysectomized animals exogenous somatotropic hormone can interfere with the effect of increased endogenous corticosterone.
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