Monocytes Stimulate Cortisol Production by Cultured Human Adrenocortical Cells

Whitcomb, Randall W.; Linehan, W. Marston; Wahl, Larry M.; Knazek, Richard A.

doi:10.1210/jcem-66-1-33

Cited by 86 publications

(26 citation statements)

References 17 publications

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“…Lastly, we did not observe type I IL-l mRNA in mouse adrenal glands, a finding at odds with some reports describing a direct effect of IL-l on adrenal cortical cells (Roh et al, 1987;Whitcomb et al, 1988;Andreis et al, 1991). However, two recent studies have failed to find any acute stimulatory effect of IL-1 on glucocorticoid secretion at the level of the adrenal gland (Naito et al, 1990;Harlin and Parker, 199 1).…”

Section: Discussioncontrasting

confidence: 99%

In situ histochemical localization of type I interleukin-1 receptor messenger RNA in the central nervous system, pituitary, and adrenal gland of the mouse

et al. 1992

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The cytokine interleukin-1 (IL-l) has a number of biologic activities, including pronounced effects on the nervous and neuroendocrine systems. In this study, in situ histochemical techniques were used to investigate the distribution of cells expressing type I IL-1 receptor mRNA in the CNS, pituitary, and adrenal gland of the mouse. Hybridization of %-labeled antisense cRNA probes derived from a murine T-cell IL-1 receptor cDNA revealed a distinct regional distribution of the type I IL-1 receptor, both in brain and in the pituitary gland. In the brain, an intense signal was observed over the granule cell layer of the dentate gyrus, over the entire midline raphe system, over the choroid plexus, and over endothelial cells of postcapillary venules throughout the neuraxis. A weak to moderate signal was observed over the pyramidal ceil layer of the hilus and CA3 region of the hippocampus, over the anterodorsal thalamic nucleus, over Purkinje cells of the cerebellar cortex, and in scattered clusters over the externalmost layer of the median eminence.In the pituitary gland, a dense and homogeneously distributed signal was observed over the entire anterior lobe. No autoradiographic signal above background was observed over the posterior and intermediate lobes of the pituitary, or over the adrenal gland. This study therefore provides evidence for discrete receptor substrates subserving the central effects of IL-l, thus supporting the notion that IL-1 acts as a neurotransmitter/neuromodulator in brain. It also supports studies suggesting that IL-1 -mediated activation of the hypothalamic-pituitary-adrenal axis occurs primarily at the level of the brain and/or pituitary gland.Interleukin-1 (IL-l) is one of a growing number of cytokines that mediate important regulatory interactions between lymphocytes and many other cell types (see Dinarello, 1989). IL-l has also been identified as a key mediator in the acute-phase

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Section: Discussioncontrasting

confidence: 99%

In situ histochemical localization of type I interleukin-1 receptor messenger RNA in the central nervous system, pituitary, and adrenal gland of the mouse

et al. 1992

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“…One pathogenic mechanism might relate to perturbations in the homeostatic interplay between the HPA axis and the immune system, in the form of cytokines (Jenkins and Grossman, 1997). It has been clearly established that interleukins (ILs) 1α, IL-1β, IL-6 and IL-2 are all able to exert a direct stimulatory effect on adrenocortical cortisol secretion (Roh et al, 1987;Whitcomb et al, 1988;Salas et al, 1990;Tominaga et al, 1991;O'Connell et al, 1994), with the stimulatory effects of IL-1α and IL-1β being suggested to be mediated via prostaglandins (PGD 2 , PGF 2 and PGE 2 ) (Winter et al, 1990;Tominaga et al, 1991). Furthermore, IL-6 has been shown to act synergistically with physiological concentrations of ACTH in stimulating cortisol secretion (Salas et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Adrenal enlargement and failure of suppression of circulating cortisol by dexamethasone in patients with malignancy

et al. 1999

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The aim of this study was to further elucidate the activity of the hypothalamo–pituitary–adrenal (HPA) axis in patients with malignancy and to correlate this with the size of the adrenal glands. Fourteen patients with a variety of malignancies were studied prior to receiving cytotoxic chemotherapy. During routine staging computerized tomographic (CT) scans, the size of the body, medial and lateral limbs of the adrenal glands were measured and compared with those of a normal group of patients studied previously. Measurements of 09:00 h serum cortisol and plasma adrenocorticotropic hormone (ACTH) levels were made before and after the administration of dexamethasone (0.5 mg 6-hourly for 48 h) in addition to the peak cortisol response to i.v corticotropin releasing hormone (CRH). Overall, patients with malignancy had significantly larger adrenal glands than patients without malignancy; those with non-haematological malignancies had larger glands than patients with haematological malignancies. Following dexamethasone to suppress circulating cortisol levels, nine patients (64%) demonstrated abnormal resistance with cortisol levels > 50 nmol l −1 : mean value 294 nmol l −1 (range 67–1147). Those patients who failed to suppress after dexamethasone had significantly larger adrenal glands than those that did suppress and tended to have non-haematological malignancies. ACTH levels were undetectable or low in three patients in whom it was measured and who did not suppress with dexamethasone. Following CRH, the cortisol levels were highest (823 and 853 nmol l −1 ) in two of these patients. Malignancy is associated with diffuse enlargement of the adrenal glands and resistance to dexamethasone-induced suppression of the HPA axis, which is not due to ectopic ACTH secretion. This disturbance of the normal control of the HPA axis is unexplained and its functional significance remains uncertain. © 1999 Cancer Research Campaign

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“…Particularly, the inflammatory cytokines TNF␣, IL-1, and IL-6 all seem to play a role in local immune-adrenal regulation. IL-1 induced corticosteroid biosynthesis in vivo independently from ACTH and caused glucocorticoid secretion in hypophysectomized rats (55), perfused rat adrenals (56), and dispersed human adrenal cells (57). IL-6 stimulated corticosterone release from rat adrenocortical cells alone and in synergy with ACTH, an effect probably mediated and amplified by PGs (58).…”

Section: Immune-adrenal Interactionsmentioning

confidence: 99%

Adrenocorticotropin (ACTH)- and Non-ACTH-Mediated Regulation of the Adrenal Cortex: Neural and Immune Inputs

Bornstein

Chrousos

1999

The Journal of Clinical Endocrinology & Metabolism

276

121

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The maintenance of life depends on the capacity of the body to sustain its steady state or homeostasis; hence, the survival of the organism relies on its ability to react and adapt to the constant bombardment by physical and emotional threats or stressors (1, 2). To accomplish this, all living beings have developed an efficient but complex adaptive response system that allows the integration of the necessary defense mechanisms directed against both external and internal stressors. This coordinated response, the stress response, involves the nervous, endocrine, and immune systems. A qualitatively and quantitatively appropriate and time-limited stress response is a prerequisite for a healthy life. Inappropriate or inappropriately excessive and chronic hyperactivation of the stress system may lead to disease and, eventually, premature death.The two major peripheral limbs of the stress system are the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (1, 2). Their central components are, respectively, located in the hypothalamus and the brain stem. Stress-induced activation of the HPA axis is associated with release of hypothalamic CRH and vasopressin (AVP), the principal regulators of anterior pituitary corticotropin (ACTH) secretion, into the hypophyseal portal system. These hormones synergistically stimulate systemic ACTH secretion, which, in turn, stimulates the adrenal cortexes to secrete glucocorticoids. Central activation of the sympathetic neurons leads to activation of both the systemic sympathetic nervous system and, through the splanchnic nerves, the adrenal medullae (3). As the proper functioning of both the HPA axis and the sympathetic nervous system is crucial for survival and maintenance of health, it is not surprising that their regulation is developmentally plastic and complex, multilevel, and redundant. The regulation and central interaction of the HPA axis and the sympathetic nervous system and the immune system have been extensively studied and summarized in recent review articles (1, 3-5). The purpose of this brief review is to outline and discuss recent advances in the interactions and regulation of the adjacent peripheral limbs of the stress system, particularly the adrenal cortex and medulla, and to point out their implications for clinical endocrinology (Fig. 1).The adrenal gland has an astonishing capacity to adapt to various forms of acute and chronic stress (6 -8). After central activation of the HPA axis, ACTH triggers a physiologic, molecular, and morphological response of the adrenal cortex. This leads not only to glucocorticoid release, but also to up-regulation of steroidogenic cytochrome P 450 messenger ribonucleic acids (9, 10) and to conspicuous structural changes in the adrenal gland characterized by both hypervascularization and cellular hypertrophy and hyperplasia (11,12). These morphological changes are mirrored on the ultrastructural level; adrenocortical cells increase the number of their mitochondria, whereas their inner membranes form a dense vesi...

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Monocytes Stimulate Cortisol Production by Cultured Human Adrenocortical Cells

Cited by 86 publications

References 17 publications

In situ histochemical localization of type I interleukin-1 receptor messenger RNA in the central nervous system, pituitary, and adrenal gland of the mouse

In situ histochemical localization of type I interleukin-1 receptor messenger RNA in the central nervous system, pituitary, and adrenal gland of the mouse

Adrenal enlargement and failure of suppression of circulating cortisol by dexamethasone in patients with malignancy

Adrenocorticotropin (ACTH)- and Non-ACTH-Mediated Regulation of the Adrenal Cortex: Neural and Immune Inputs

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