Synergistic roles of interleukin-6, interleukin-1, and tumor necrosis factor in the adrenocorticotropin response to bacterial lipopolysaccharide in vivo

Perlstein, Robert S.

doi:10.1210/en.132.3.946

Cited by 120 publications

(61 citation statements)

References 1 publication

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“…The acute stress response is associated with a hyper-corticotropin, hypercortisol state, driven by elevated hypothalamic corticotropin-releasing hormone levels and by the known effects of tumor necrosis factor-a, interleukin-1b and interleukin-6 on corticotropin-releasing hormone and corticotropin [61][62][63]. Cytokine secretion inhibits normal negative feedback.…”

Section: Pituitary-adrenal Axismentioning

confidence: 99%

The inflammatory response to surgery and trauma

Kohl

Deutschman

2006

Current Opinion in Critical Care

176

132

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Section: Pituitary-adrenal Axismentioning

confidence: 99%

The inflammatory response to surgery and trauma

Kohl

Deutschman

2006

Current Opinion in Critical Care

176

132

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“…Moreover, CRH release from hypothalamic explants is increased by IL-6 treatment [10, 11]. Lipopolysaccharide (LPS)-induced ACTH release is partly abrogated in IL-6-immunoneutralized rats and in IL-6-deficient mice [12, 13]. These data suggest that IL-6 is an important mediator of LPS-induced ACTH; however, its mechanisms of action are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

In vivo Activation of the Interleukin-6 Receptor/gp130 Signaling Pathway in Pituitary Corticotropes of Lipopolysaccharide-Treated Rats

Gautron¹,

Lafon²,

Tramu³

et al. 2003

Neuroendocrinology

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Adrenocorticotropic hormone (ACTH) release from anterior pituitary corticotropes is greatly increased during peripheral inflammation induced by lipopolysaccharide (LPS) administration. Interleukin-6 (IL-6) is thought to participate in LPS-induced ACTH release, but whether or not corticotropes are directly targeted by this cytokine is unclear. Therefore, we investigated the expression and activation of IL-6 signaling components in the pituitary of rats 2 and 4 h after administration of LPS (250 µg/kg). Intraperitoneal LPS treatment provoked the nuclear translocation of signal transducer and activator of transcription 3 (STAT-3) and Fos expression in the anterior pituitary lobe, as demonstrated by immunohistochemistry. By using in situ hybridization, we demonstrated that suppressor of cytokine signaling 3 (SOCS-3) and c-fos mRNAs were significantly induced by the LPS treatment in the anterior lobe of the pituitary. Dual in situ hybridization revealed that most corticotropes expressed IL-6 receptor and gp130 mRNAs, and that 2 h after LPS treatment, SOCS-3 and c-fos mRNAs were induced in corticotropes. Our results suggest that LPS-induced IL-6 could regulate the hypothalamo-pituitary-adrenal axis by directly targeting corticotropes during peripheral inflammation.

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“…AI may be part of APassociated multi-organ dysfunctions [31] and may have some association with the rapid progression and destruction of necrotizing pancreas [15], high incidence of complications, and high mortality in pancreatitis [4]. Exhaustion of adrenal cortex has been considered as responsible for AI in the early last century and proposed possible mechanisms for adrenal suppression during inflammation include direct inhibition of ACTH stimulation on adrenal cells, decreased pituitary response to CRH, interference with cortisol binding, release of adrenal contents of cAMP, and diminished adrenal blood flow [40][41][42][43][44]. In addition, the damage to adrenal cortex due to adrenal hemorrhage, necrosis, or adrenal vein thrombosis in some kinds of sepsis in coagulation disorders may be the direct explanations of AI [35,45,46].…”

Section: Discussionmentioning

confidence: 99%

Changes of Inflammation and Apoptosis in Adrenal Gland After Experimental Injury in Rats with Acute Necrotizing Pancreatitis

Wang

et al. 2010

Inflammation

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We hypothesize that adrenal insufficiency in acute necrotizing pancreatitis (ANP) is attributable to hemorrhagic inflammation, necrosis, and apoptosis of the adrenal cortex. Arguments to support this view are presented in the study that investigated morphological and functional changes of adrenal and the distinct roles of inflammatory mediator secretory phospholipase A(2) (sPLA(2)) and apoptosis-related genes Bax and Bcl-2 played in acute adrenal injury in ANP. After ANP model was induced, pancreatic histology, serum amylase, sPLA(2), and corticosterone were analyzed. The adrenal morphology, apoptotic cells by TUNEL assay, and ultrastructures were observed. sPLA(2)-IIA and Bcl-2 and Bax expressions were detected by immunohistochemistry. Histopathologic grading of adrenal was higher in ANP group than in controls. Serum corticosterone was stimulated to maximal level at 3 h, then dropped to the bottom at 24 h (P<0.05). Apoptotic index, sPLA2-IIA, and Bax expression were increased steeply after pancreatitis, and the Bax/Bcl-2 ratio was elevated gradually (P<0.05). Sustained decrease in serum corticosterone level following adrenal injury during ANP appears to be, in part, due to the crucial roles of inflammation and apoptosis in adrenal cortex. These findings could suggest that sPLA2, Bax, and Bcl-2 may be involved in the course of adrenal injury after ANP.

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Synergistic roles of interleukin-6, interleukin-1, and tumor necrosis factor in the adrenocorticotropin response to bacterial lipopolysaccharide in vivo

Cited by 120 publications

References 1 publication

The inflammatory response to surgery and trauma

The inflammatory response to surgery and trauma

In vivo Activation of the Interleukin-6 Receptor/gp130 Signaling Pathway in Pituitary Corticotropes of Lipopolysaccharide-Treated Rats

Changes of Inflammation and Apoptosis in Adrenal Gland After Experimental Injury in Rats with Acute Necrotizing Pancreatitis

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