Environmental modulation of the immune system via the endocrine system.
Numerous studies have demonstrated that a variety of hormones have receptors and exert biologic actions on tissues of the immune system. Conversely, cytokines exert biologic actions on the endocrine system. This bidirectional interaction is likely involved in maintenance of physiological and immunologic homeostasis. This paper summarizes a variety of actions of growth hormone (GH), prolactin (PRL), insulin-like growth factor-I (IGF-I), glucocorticoids and thyroid hormones (TH) on the immune system. It then proceeds to put these actions into a hypothetical context whereby these hormones may mediate some changes in immune system function in response to environmental stimuli such as physical and emotional stress, nutritional deprivation and environmental temperature. In the first example, it is proposed that PRL secretion in response to stress may serve an immunomodulatory role in two ways. The first is by stimulating the immune system directly and the second is by dampening or reducing the degree to which glucocorticoids are secreted in response to stress. The second example suggests that the increase in GH secretion and reduced IGF-I secretion in response to protein/energy restriction may have two potential immunomodulatory actions. One action is a direct effect of GH on several components of the immune system. The other is the partitioning of nutrient use away from skeletal muscle growth and toward tissues of higher priority such as the immune system. The third example proposes that the increased secretion of TH during cold environmental temperatures not only increases basic metabolic rate, but also directly stimulates both primary and secondary lymphoid tissues. It is suggested, therefore, that these three hormones are involved in maintaining immune system homeostasis in response to environmental change.
Davis
S L
SL
Department of Animal Sciences, Oregon State University, Corvallis 97331, USA.
D000818:Animals; D003080:Cold Temperature; D016207:Cytokines / Q000276:immunology / Q000502:physiology*; D004703:Endocrine System / Q000276:immunology* / Q000502:physiology; D005246:Feedback / Q000502:physiology; D005938:Glucocorticoids / Q000378:metabolism; D013006:Growth Hormone / Q000378:metabolism; D006728:Hormones / Q000276:immunology* / Q000502:physiology; D007030:Hypothalamo-Hypophyseal System / Q000276:immunology / Q000502:physiology; D007107:Immune System / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D009752:Nutritional Status / Q000276:immunology / Q000502:physiology; D010913:Pituitary-Adrenal System / Q000276:immunology / Q000502:physiology; D011388:Prolactin / Q000378:metabolism; D013312:Stress, Physiological / Q000276:immunology / Q000503:physiopathology; D013963:Thyroid Hormones / Q000276:immunology / Q000502:physiology
D016207:Cytokines; D005938:Glucocorticoids; D006728:Hormones; D013963:Thyroid Hormones; D007334:Insulin-Like Growth Factor I; D011388:Prolactin; D013006:Growth Hormone