Effects of cytokines on pituitary β-endorphin and adrenal corticosterone release in vitro

Meer, M.J.M. van der; Hermus, A.R.M.M.; Pesman, G. J.; Sweep, Fred C.G.J.

doi:10.1006/cyto.1996.0033

Cited by 31 publications

(12 citation statements)

References 19 publications

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“…injection of IL‐1 β in rats, without affecting the corticosterone response ( 50). In vitro studies on adrenocortical tissue or primary culture of adrenocortical cells demonstrated a dose‐dependent stimulatory action of IL‐1 β on corticosterone secretion ( 51, 52). Furthermore, this direct action of IL‐1 β on the adrenal cortex seems to depend on the eicosanoids pathway.…”

Section: Discussionmentioning

confidence: 99%

Effects of the Inhibition of Cyclo‐Oxygenase 1 or 2 or 5‐Lipoxygenase on the Activation of the Hypothalamic‐Pituitary‐Adrenal Axis Induced by Interleukin‐1β in the Male Rat

Parsadaniantz

Lebeau

Duval

et al. 2000

J Neuroendocrinology

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The limited entry of interleukin-1beta (IL-1beta) into the central nervous system has led to the hypothesis that IL-1beta acts, through IL-1beta receptors located notably on endothelial cells, on the release of prostaglandins which in turn stimulate the hypothalamic-pituitary-adrenal (HPA) axis. We used cyclo-oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) inhibitors, before the injection of IL-1beta, to explore the role of arachidonic acid metabolic pathways on HPA axis activation. Adult male rats were i.m injected 20 min before i.p injection of IL-1beta, with (i): a COX-1/COX-2 inhibitor (ketoprofen); (ii) a COX-2 selective inhibitor (NS 398); or (iii) a 5-LOX inhibitor (BW A4C). Following this, rats were killed 90 min after i.p. IL-1beta injection and analysis for plasma adrenocorticotropic hormone (ACTH) and corticosterone concentrations and determination of anterior pituitary pro-opio melanocortin (POMC) gene transcription was conducted. Administration of the COX-1/COX-2 inhibitor led to a complete blockage of ACTH and corticosterone secretion and POMC gene transcription. The COX-2 inhibitor led to a complete blockade of ACTH secretion and POMC gene transcription but had no effect on corticosterone secretion. The 5-LOX inhibitor had no significant effect on any parameter. These results demonstrate the crucial role of eicosanoid pathways in mediating the stimulation of the HPA axis induced by IL-1beta. Moreover, we found a clear dissociation of the effect of the blockage of COXs upon ACTH and corticosterone secretion, suggesting that IL-1beta may act at the brain as well as at the adrenal cortex to stimulate the secretion of corticosterone.

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Section: Discussionmentioning

confidence: 99%

Effects of the Inhibition of Cyclo‐Oxygenase 1 or 2 or 5‐Lipoxygenase on the Activation of the Hypothalamic‐Pituitary‐Adrenal Axis Induced by Interleukin‐1β in the Male Rat

Parsadaniantz

Lebeau

Duval

et al. 2000

J Neuroendocrinology

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“…van der Meer et al found that IL-2 had no significant effect on glucocorticoid secretion from isolated rat adrenal cells within 60 min, but a small stimulation was apparent approximately 4 h after completion of a 6 h incubation with IL-1b. 20 In vitro studies have indicated that IL-1b does not influence either basal or ACTH-stimulated glucocorticoid production from human fetal adrenal tissue either in cell or in organ culture. 21 However, IL-1b increases glucocorticoid secretion from rat adrenal glands, 22 and rat as well as human dispersed adrenal cells.…”

Section: Discussionmentioning

confidence: 99%

“…22,23 These studies indicated that the important causes for the different findings related to the direct action of IL-1b on adrenal glucocorticoid secretion may be the various adrenal cell preparations and different incubation times. 11,[20][21][22][23] Therefore, in the issue of whether IL-15 directly inhibits CORT secretion in vitro, the influence of the period of incubation is of interest. In this study, we used three incubation periods (30, 60 and 120 min) for reporting the effect of IL-15 on CORT secretion in rat ZFR cells.…”

Section: Discussionmentioning

confidence: 99%

Direct effects of IL‐15 on corticosterone secretion by rat adrenocortical cells

Lee

2005

Immunol Cell Biol

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Summary Cytokines might regulate the function of the hypothalamic-pituitary-adrenal axis. IL-15 is a potent non-T-cell-derived cytokine with IL-2-like activities. It has been shown that IL-15 can reverse the inhibition of glucocorticoids on PBMC. In vitro experiments were designed to assess the direct effect of IL-15 on corticosterone (CORT) secretion in the adrenal zona fasciculata-reticularis (ZFR) cells of male rats. Administration of IL-15 dose dependently decreased the basal and adrenocorticotropin-stimulated release of CORT and production of cAMP in ZFR cells. The stimulatory effect of forskolin (an adenylate cyclase activator) on CORT secretion and accumulation of cAMP in ZFR cells was attenuated by the administration of IL-15. However, 8-Br-cAMP (a cAMP analogue)-stimulated release of CORT was not affected by IL-15. Exogenous administration of IL-15 (10 ÿ7 mol/L) significantly attenuated the pregnenolone (the substrate of 3b-hydroxysteroid dehydrogenase)-or deoxycorticosterone (the substrate of 11b-hydroxylase)-induced release of CORT. The results indicate that decrease of CORT secretion by IL-15 is in part because of (i) the decrease of adenylate cyclase activity and cAMP production and (ii) the inhibition of 3b-hydroxysteroid dehydrogenase and 11b-hydroxylase activities in rat ZFR cells.

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“…The stimulatory influence of the proinflammatory cytokine on the ACTH release is blunted in animals bearing a bilateral lesion of the hypothalamic PVN suggesting that neuroendocrine CRF mediates ACTH‐inducing activity of TNF (87). Other studies have also provided evidence that the acute activation of the pituitary‐adrenal axis following in vivo IL‐1, IL‐6, and TNF administration is not mediated by a direct action of these cytokines at the level of the pituitary and/or adrenal gland (88). Our data that intravenous TNF‐α‐activated transcription of the neuroendocrine CRF and the strong expression of the IEG c‐ fos in the paravocellular PVN are clear evidence that the neurons controlling the HPA axis are activated by the circulating cytokine (85).…”

Section: Tumor Necrosis Factor‐αmentioning

confidence: 99%

How the Blood Talks to the Brain Parenchyma and the Paraventricular Nucleus of the Hypothalamus During Systemic Inflammatory and Infectious Stimuli

Rivest

Lacroix

Vallières

et al. 2000

Proc Soc Exp Biol Med

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Abstract. There are exciting new developments regarding the molecular mechanisms involved in the influence of circulating proinflammatory molecules within cells of the blood‐brain barrier (BBB) during systemic immune challenges. These molecules, when present in the circulation, have the ability to trigger a series of events in cascade, leading to either the mitogen‐activated protein (MAP) kinases/nuclear factor kappa B (NF‐κB) or the janus kinase (JAK)/signal transducer and activator of transcription (STAT) transduction pathways in vascular‐associated cells of the central nervous system (CNS). The brain blood vessels exhibit both constitutive and induced expression of receptors for different proinflammatory ligands that have the ability to stimulate these signaling molecules. Depending on the challenges and the cytokines involved, the transduction signal(s) solicited in cells of the BBB may orient the neuronal activity in a very specific manner in activating the transcription and production of soluble factors, such as prostaglandins (PGs). It is interesting to note that cytokines as well as systemic localized inflammation stimulate the cells of the BBB in a nonselective manner (i.e., within both large blood vessels and small capillaries across the brain). This nonselectivity raises several questions with regard to the localized neuronal activation induced by different experimental models of inflammation and cytokines. It is possible that the selectivity of the neuronal response is a consequence of the fine interaction between nonparenchymal synthesis of soluble mediators and expression of specific receptors for these ligands within parenchymal elements of different brain nuclei. This review will present the recent developments on this concept and the mechanisms that take place in cells of the BBB, which lead to the neuronal circuits involved in restoring the body's homeostasis during systemic immunogenic challenges. The induction of fever, the hypothalamic‐pituitary adrenal (HPA) axis, and other autonomic functions are among the physiological outcomes necessary for the protection of the mammalian organism in the presence of foreign material.

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Effects of cytokines on pituitary β-endorphin and adrenal corticosterone release in vitro

Cited by 31 publications

References 19 publications

Effects of the Inhibition of Cyclo‐Oxygenase 1 or 2 or 5‐Lipoxygenase on the Activation of the Hypothalamic‐Pituitary‐Adrenal Axis Induced by Interleukin‐1β in the Male Rat

Effects of the Inhibition of Cyclo‐Oxygenase 1 or 2 or 5‐Lipoxygenase on the Activation of the Hypothalamic‐Pituitary‐Adrenal Axis Induced by Interleukin‐1β in the Male Rat

Direct effects of IL‐15 on corticosterone secretion by rat adrenocortical cells

How the Blood Talks to the Brain Parenchyma and the Paraventricular Nucleus of the Hypothalamus During Systemic Inflammatory and Infectious Stimuli

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