Hypothalamic Pituitary Adrenal Axis and Immune Responses to Endotoxin in Rats with Chronic Adjuvant-Induced Arthritis

Grinevich, Valery; Harbuz, Michael S.; Ma, Xin−Ming; Jessop, David S.; Tilders, F. J. H.; Lightman, Stafford L.; Aguilera, Greti

doi:10.1006/exnr.2002.8022

Cited by 20 publications

(11 citation statements)

References 45 publications

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“…Previous reports have shown that in the basal state cytokines are expressed in low abundance in the brain and that IL-6 is colocalized with vasopressin (22,23,32). Consistent with both these notions, when we examined IL-6 immunoreactivity in the hypothalamus of pigs, we observed faint immunoreactivity in vasopressinergic neurons (data not shown).…”

Section: Discussionsupporting

confidence: 89%

“…Consistent with both these notions, when we examined IL-6 immunoreactivity in the hypothalamus of pigs, we observed faint immunoreactivity in vasopressinergic neurons (data not shown). IL-6 mRNA has been detected in response to lipopolysaccharide in the paraventricular nucleus (PVN) and the median eminence/arcuate region (32). Additionally, in response to dehydration, IL-6 mRNA was detected in the PVN and supraoptic nucleus (23).…”

Section: Discussionmentioning

confidence: 99%

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Sex Difference in Link between Interleukin-6 and Stress

et al. 2007

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Inflammation contributes to disease development, and the neuroimmunoendocrine interface is a potential site of action for inflammatory products like IL-6 to affect health. Although plasma IL-6 can stimulate the activity of the hypothalamo-pituitary-adrenocortical (HPA) axis, the precise role, if any, for IL-6 in the HPA response to nonimmunological stressors is unclear. The purpose of this study was to test the hypothesis that IL-6 in the stalk median eminence (SME) can be directly involved in stimulating ACTH secretion in response to acute stress in female swine. This study was undertaken as a result of finding IL-6 localized to the external zone of the SME next to the hypophyseal portal vessels. Results indicate that content of IL-6 in the SME decreases in response to acute stress along with an increase in nuclear phosphorylated signal transducer and activator of transcription-3 (pSTAT-3) in pituitary corticotrophs and a simultaneous increase in plasma concentrations of IL-6 and ACTH. Furthermore, we show that females concomitantly display greater SME content of IL-6 and greater HPA responsiveness to stress, thereby suggesting that IL-6 release from the SME is an integral factor contributing to enhanced stress responsiveness in females. Our results provide evidence for a direct link between IL-6 and ACTH release and reveal a sex difference in this relationship.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Sex Difference in Link between Interleukin-6 and Stress

et al. 2007

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“…Numerous studies have revealed a plethora of factors other than CRH involved in the suppression of reproductive function by stressful stimuli. For example, VP is co-expressed with CRH in the PVN upon chronic activation of the HPA axis (Plotsky, 1991; Aguilera, 1998; Grinevich et al, 2002), implying an involvement of this neuropeptide in stress. Several studies have demonstrated that VP can affect LH release: for example, infusion of VP into the lateral ventricles attenuates the preovulatory LH surge in rats (DePaolo et al, 1986) and causes a transient inhibition (although with lower potency than CRH) of LH release in male rats (Rivier and Vale, 1985).…”

Section: Discussionmentioning

confidence: 99%

Deciphering the Contributions of CRH Receptors in the Brain and Pituitary to Stress-Induced Inhibition of the Reproductive Axis

Raftogianni

Roth

García‐González

et al. 2018

Front. Mol. Neurosci.

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Based on pharmacological studies, corticotropin-releasing hormone (CRH) and its receptors play a leading role in the inhibition of the hypothalamic–pituitary–gonadal (HPG) axis during acute stress. To further study the effects of CRH receptor signaling on the HPG axis, we generated and/or employed male mice lacking CRH receptor type 1 (CRHR1) or type 2 (CRHR2) in gonadotropin-releasing hormone neurons, GABAergic neurons, or in all central neurons and glia. The deletion of CRHRs revealed a preserved decrease of plasma luteinizing hormone (LH) in response to either psychophysical or immunological stress. However, under basal conditions, central infusion of CRH into mice lacking CRHR1 in all central neurons and glia, or application of CRH to pituitary cultures from mice lacking CRHR2, failed to suppress LH release, unlike in controls. Our results, taken together with those of the earlier pharmacological studies, suggest that inhibition of the male HPG axis during acute stress is mediated by other factors along with CRH, and that CRH suppresses the HPG axis at the central and pituitary levels via CRHR1 and CRHR2, respectively.

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“…Acute LPS administration raised the expression of both AVP and CRH. However, both types of immune challenges increased ACTH and corticosterone levels (Grinevich et al , 2002). …”

Section: 0 Inflammation and Depressionmentioning

confidence: 99%

Eating ourselves to death (and despair): The contribution of adiposity and inflammation to depression

Shelton

Miller

2010

Progress in Neurobiology

207

148

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Obesity and related metabolic conditions are of epidemic proportions in most of the world, affecting both adults and children. The accumulation of lipids in the body in the form of white adipose tissue in the abdomen is now known to activate innate immune mechanisms. Lipid accumulation causes adipocytes to directly secrete the cytokines interleukin (IL) 6 and tumor necrosis factor α (TNFα), but also monocyte chemoattractant protein 1 (MCP-1), which results in the accumulation of leukocytes in fat tissue. This sets up a chronic inflammatory state which is known to mediate the association between obesity and conditions such as cardiovascular disease, type 2 diabetes, and cancer. There is also a substantial literature linking inflammation with risk for depression. This includes the observations that: 1. People with inflammatory diseases such as multiple sclerosis, cardiovascular disease, and psoriasis have elevated rates of depression; 2. Many people administered inflammatory cytokines such as interferon α develop depression that is indistinguishable from depression in non-medically ill populations; 3. A significant proportion of depressed persons show upregulation of inflammatory factors such as IL-6, C-reactive protein, and TNFα; and 4) Inflammatory cytokines can interact with virtually every pathophysiologic domain relevant to depression, including neurotransmitter metabolism, neuroendocrine function, and synaptic plasticity. While many factors may contribute to the association between inflammatory mediators and depression, we hypothesize that increased adiposity may be one causal pathway. Mediational analysis suggests a bi-directional association between adiposity and depression, with inflammation possibly playing an intermediary role.

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Hypothalamic Pituitary Adrenal Axis and Immune Responses to Endotoxin in Rats with Chronic Adjuvant-Induced Arthritis

Cited by 20 publications

References 45 publications

Sex Difference in Link between Interleukin-6 and Stress

Sex Difference in Link between Interleukin-6 and Stress

Deciphering the Contributions of CRH Receptors in the Brain and Pituitary to Stress-Induced Inhibition of the Reproductive Axis

Eating ourselves to death (and despair): The contribution of adiposity and inflammation to depression

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