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Abstract

Protection against stress by glucocorticoids is discussed in relation to their permissive and suppressive actions. Evidence from the last decade is summarized regarding the physiological nature of the suppressive actions, and the hypothesis that they prevent stress-activated defense mechanisms from overshooting and damaging the organism. Support for this hypothesis has come from observations on how endogenous or administered glucocorticoids control inflammatory and immune responses, protect in endotoxic and hemorrhagic shock, regulate central nervous system responses to stimuli, and moderate many defense reactions through suppression of cytokines and other mediators. Studies showing that glucocorticoids permissively induce receptors for several mediators that they suppress have led to a model in which stimulated activity of a mediator system is increased permissively through induction of mediator receptors and decreased through suppression of mediator production.

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Endogenous glucocorticoids regulate an inducible cyclooxygenase enzyme.

K Seibert, J Masferrer, P Needleman … (1992)

The effect of endogenous glucocorticoids on the expression of the cyclooxygenase enzyme was studied by contrasting cyclooxygenase expression and prostanoid synthesis in adrenalectomized and sham-adrenalectomized mice with or without the concurrent administration of endotoxin. Peritoneal macrophages obtained from adrenalectomized mice showed a 2- to 3-fold induction in cyclooxygenase synthesis and activity when compared to sham controls. Intravenous injection of a sublethal dose of endotoxin (5 micrograms/kg) further stimulated cyclooxygenase synthesis, resulting in a 4-fold increase in prostaglandin production. Similar cyclooxygenase induction can be achieved in macrophages obtained from normal mice but only after high doses of endotoxin (2.5 mg/kg) that are 100% lethal to adrenalectomized mice. Restoration of glucocorticoids in adrenalectomized animals with dexamethasone completely inhibited the elevated cyclooxygenase and protected these animals from endotoxin-induced death. In contrast, no signs of cyclooxygenase induction were observed in the kidneys of the adrenalectomized mice, even when treated with endotoxin. Dexamethasone did not affect the constitutive cyclooxygenase activity and prostaglandin production present in normal and adrenalectomized kidneys. These data indicate the existence of a constitutive cyclooxygenase that is normally present in most cells and tissues and is unaffected by steroids and of an inducible cyclooxygenase that is expressed only in the context of inflammation by proinflammatory cells, like macrophages, and that is under glucocorticoid regulation. Under normal physiological conditions glucocorticoids maintain tonic inhibition of inducible cyclooxygenase expression. Depletion of glucocorticoids or the presence of an inflammatory stimulus such as endotoxin causes rapid induction of this enzyme, resulting in an exacerbated inflammatory response that is often lethal.

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Glucocorticoids and Immune Function

ALLAN MUNCK, PAUL M. GUYRE (1991)

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Glucocorticoid sensitivity of vasopressin mRNA levels in the paraventricular nucleus of the rat.

L G Davis, R Arentzen, J Reid … (1986)

Immunocytochemical studies have shown that adrenalectomy produces changes in the content and distribution of [arginine-8]vasopressin (AVP) immunoreactivity in the paraventricular nucleus of the hypothalamus. The purpose of this study was to determine whether manipulation of adrenal hormones affects the levels of AVP mRNA. In situ hybridization assays with highly specific synthetic oligodeoxyribonucleotide probes and immunocytochemistry were used to detect the distribution of AVP mRNA and AVP-immunoreactive perikarya. AVP mRNA is codistributed with AVP immunoreactivity in the posterior magnocellular subdivision of the paraventricular nucleus and its accessory nuclei, the supraoptic nucleus and the suprachiasmatic nucleus. In adrenalectomized rats, the density and distribution of the hybridization signal were increased in the paraventricular nucleus; a 2-fold increase in the area comprising the signal was observed. At the cellular level, silver grains were detected in corticotropin-releasing-factor-immunoreactive neurons throughout the medial parvocellular subdivision of the paraventricular nucleus. No changes were seen in the distribution of AVP mRNA in the supraoptic or suprachiasmatic nuclei. Treatment with dexamethasone prevented the increase in AVP mRNA produced by adrenalectomy. In contrast, adrenalectomy did not alter the hybridization signal obtained with a probe for alpha-tubulin mRNA. These results suggest, at the cellular level, that adrenalectomy induces a glucocorticoid-sensitive stimulation of AVP mRNA synthesis in the central nervous system. Thus, considerable plasticity in gene expression is retained in the hypothalamus of the adult rat.

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PubMed ID:: 7825870

ScienceOpen disciplines: Chemistry

Keywords: Animals,Anti-Inflammatory Agents,pharmacology,Brain,drug effects,physiology,Cytokines,Glucocorticoids,Homeostasis,Humans,Immunosuppressive Agents,Models, Biological,Shock,physiopathology,Steroids,Stress, Physiological

Glucocorticoids and stress: permissive and suppressive actions.

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Most cited references 7

Endogenous glucocorticoids regulate an inducible cyclooxygenase enzyme.

Glucocorticoids and Immune Function

Glucocorticoid sensitivity of vasopressin mRNA levels in the paraventricular nucleus of the rat.

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