The ups and downs of glucocorticoid physiology Permissive and suppressive effects revisited

Munck, Allan; Náray-Fejes-Tóth, Anikó

doi:10.1016/0303-7207(92)90091-j

Cited by 156 publications

(95 citation statements)

References 13 publications

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“…In the case of the hemorrhage, the first wave of neuroendocrine response also includes massive secretion of arginin vasopression (AVP) from the pituitary and renin from the kidney (Hench et al 1950;Munck et al 1984;Marzinzig et al 1997;Sabatini et al 2005). From hours to days after the stress, glucocorticoid hormone and sympatho-adreno-medullary system play important roles in coresponding with each other (Ingle 1952;Orchinik et al 1991;Munck and Naray-Fejes-Toth 1992). Our data supported these findings, and excretion of catecholamines and 17-OHCS in the first day had significant positive correlation with the severities of burn.…”

Section: Discussionsupporting

confidence: 78%

Neuroendocrine System Response Modulates Oxidative Cellular Damage in Burn Patients

Xie

Shinozawa

Sasaki

et al. 2007

Tohoku J. Exp. Med.

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Oxygen-derived free radicals play important roles in pathophysiological processes in critically ill patients, but the data characterizing relationships between radicals and neuroendocrine system response are sparse. To search the cue to reduce the oxidative cellular damage from the point of view of neuroendocrine system response, we studied the indicators of neuroendocrine and inflammatory responses excreted in urine in 14 burn patients (42.3 ± 31.4 years old, and 32.3 ± 27.6% burn of total body surface area [%TBSA]) during the first seven days post burn. The daily mean amounts of urinary excretion of 8-hydroxy-2′-deoxy-guanosine (8-OHdG), a marker of oxidative cellular damage, were above the upper limit of the standard value during the studied period. The total amount of urinary excretion of 8-OHdG in the first day post burn correlated with burn severity indices: %TBSA (r = 0.63, p = 0.021) and burn index (r = 0.70, p = 0.008). The daily urinary excretion of 8-OHdG correlated with the daily urinary excretion of norepinephrine and nitrite plus nitrate (NOx) during the studied period except day 2 post burn, and correlated with the daily urinary excretion of 17-hydroxycorticosteriod (17-OHCS) in days 2, 3, and 7 post burn. These data suggest that oxidative cellular damage correlates with burn severity and neuroendocrine system response modulates inflammation and oxidative cellular damage. Modulation of neuroendocrine system response and inflammation in the treatment in the early phase of burn may be useful to reduce the oxidative cellular damage and to prevent multiple organ failures in patients with extensive burn. free radical; 8-OHdG; norepinephrine; 17-OHCS; nitrogen oxide

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Section: Discussionsupporting

confidence: 78%

Neuroendocrine System Response Modulates Oxidative Cellular Damage in Burn Patients

Xie

Shinozawa

Sasaki

et al. 2007

Tohoku J. Exp. Med.

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“…The evidence supporting such a permissive effect of glucocorticoids on enhancing sensitivity of various metabolic and humoral immune responses has been reviewed (39,44). For example, it is generally accepted that the permissive effects of glucocorticoids are necessary for the optimal glycogenolytic effects of catecholamines and the gluconeogenic effects of glucagon which combine to maintain glucose homeostasis under stress conditions (45).…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids and TNFα Interact Cooperatively to Mediate Sepsis-Induced Leucine Resistance in Skeletal Muscle

Lang

Frost

2006

Mol Med

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Sepsis blunts the ability of nutrient signaling by leucine to stimulate skeletal muscle protein synthesis by impairing translation initiation. The present study tested the hypothesis that overproduction of either tumor necrosis factor (TNF)-α or glucocorticoids mediate the sepsis-induced leucine resistance. Prior to producing peritonitis, rats received either vehicle, TNF binding protein (TNF BP ) to inhibit endogenous TNFα action, and/or the glucocorticoid receptor antagonist RU486. Leucine was orally administered to all rats 24 h thereafter and the gastrocnemius removed 20 min later to assess protein synthesis and signaling components important in controlling peptide-chain initiation. Muscle protein synthesis was 65% lower in septic rats administered leucine than in leucinetreated control animals. This reduction was not prevented by either TNF BP or RU486 alone, but was completely reversed by the combination. This sepsis-induced leucine resistance was associated with an 80% reduction in the amount of active eIF4E·eIF4G complex, a 5-fold increase in the formation of the inactive eIF4E·4E-BP1 complex as well as markedly reduced (at least 70%) phosphorylation of 4E-BP1, eIF4G, S6K1, S6, and mTOR. Pretreatment of septic rats with either TNF BP or RU486 individually only nominally improved the leucine action as assessed by the above-mentioned endpoints. In contrast, when TNF BP and RU486 were co-administered, the ability of sepsis to impair the leucine-stimulated phosphorylation of 4E-BP1, eIF4G, S6K1, and S6 as well as the redistribution of eIF4E was essentially prevented. No differences in the total amount or phosphorylation of eIF2α and eIF2Bε were detected between the different groups, and changes could not be attributed to differences in the prevailing plasma concentration of insulin or leucine. Our data demonstrate the sepsis-induced leucine resistance in skeletal muscle results from the cooperative interaction of both TNFα and glucocorticoids.

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“…Conversely, at high GC levels, receptors are in abundance, but cytokines are suppressed so signaling is low. Thus, cytokine signaling is minimal at extreme GC concentrations and peaks at an intermediate GC concentration (Munck and Naray-Fejes-Toth 1992). This observation has been shown to have functional importance in the proliferative effect of IL-2 signaling on T cells.…”

Section: The Pro-inflammatory Effects Of Gcs Outside the Nervous Systemmentioning

confidence: 93%

An inflammatory review of glucocorticoid actions in the CNS

Sorrells¹,

Sapolsky²

2007

Brain, Behavior, and Immunity

381

283

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In recent years the classic view that glucocorticoids, the adrenal steroids secreted during stress, are universally anti-inflammatory has been challenged at a variety of levels. It was first observed that under some circumstances, acute GC exposure could have pro-inflammatory effects on the peripheral immune response. More recently, chronic exposure to GCs has been found to have pro-inflammatory effects on the specialized immune response to injury in the central nervous system. Here we review the evidence that in some cases, glucocorticoids can increase pro-inflammatory cell migration, cytokine production, and even transcription factor activity in the brain. We consider how these unexpected effects of glucocorticoids can co-exist with their well-established anti-inflammatory properties, as well as the considerable clinical implications of these findings.

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The ups and downs of glucocorticoid physiology Permissive and suppressive effects revisited

Cited by 156 publications

References 13 publications

Neuroendocrine System Response Modulates Oxidative Cellular Damage in Burn Patients

Neuroendocrine System Response Modulates Oxidative Cellular Damage in Burn Patients

Glucocorticoids and TNFα Interact Cooperatively to Mediate Sepsis-Induced Leucine Resistance in Skeletal Muscle

An inflammatory review of glucocorticoid actions in the CNS

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