Cellular and Molecular Mechanisms of the Interaction between the Immune and Neuroendocrine Systems in Experimental Chronic Fatigue Syndrome

Rybakina, E. G.; Shanin, S. N.; Fomicheva, E. E.; Корнева, Е. А.

doi:10.1007/s11055-011-9400-2

Cited by 4 publications

(3 citation statements)

References 19 publications

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“…Some studies suggest that stress triggers depression with increasing output of glucocorticoids [39], [40]. In contrast to these papers, another theory considers that stress-induced decline in glucocorticoids output involves in the pathogenesis of depression [41]. Our results demonstrated the level of corticosterone was significantly increased in rats exposed to AS, on the contrary the rats exposed to chronic stress (CPSU or CSD) showed obviously lower level of corticosterone than naive controls.…”

Section: Discussioncontrasting

confidence: 56%

Bidirectional Crosstalk between Stress-Induced Gastric Ulcer and Depression under Chronic Stress

Zhang

Gao

et al. 2012

PLoS ONE

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Stress contributes to a variety of diseases and disorders such as depression and peptic ulcer. The present study aimed to investigate the correlation between stress ulcer and depression in pathogenesis and treatment by using chronic stress depression (CSD), chronic psychological stress ulcer (CPSU) and water immersion restrain stress models in rats. Our data showed that the ulcer index of the animals after CSD exposure was significantly higher than that of controls. Depression-like behaviors were observed in rat after CPSU exposure. Fluoxetine hydrochloride significantly reduced the ulcer index of rats exposed to CPSU stress, while ranitidine inhibited depression-like behavior of the animals in CSD group. The ulcer index of rats administered with mifepristone after CPSU stress was markedly reduced compared to CPSU group, although there was no significant difference in the depression-like behavior between mifepristone-treated CSD group and naive controls. We also found that the rats exposed to CPSU or CSD stress displayed a lower level of corticosterone than naive controls, however, the acute stress (AS) group showed an opposite result. Additionally, in order to study the relevance of H2 receptors and depression, we treated the CSD group with cimetidine and famotidine respectively. The data showed that cimetidine inhibited depression-like behavior in CSD rats, and famotidine had no impact on depression. Overall our data suggested that the hypothalamic-pituitary-adrenal (HPA) axis dysfunction may be the key role in triggering depression and stress ulcer. Acid-suppressing drugs and antidepressants could be used for treatment of depression and stress ulcer respectively. The occurrence of depression might be inhibited by blocking the central H2 receptors.

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Section: Discussioncontrasting

confidence: 56%

Bidirectional Crosstalk between Stress-Induced Gastric Ulcer and Depression under Chronic Stress

Zhang

Gao

et al. 2012

PLoS ONE

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“…These inflammatory cytokines have also been implicated in a number of clinical conditions involving a primary component of fatigue or malaise, including chronic fatigue syndrome and multiple chemical sensitivity [ 86 , 87 ]. In fact, disturbances of hypothalamic neuroendocrine activity and elevations of brain cytokines which are evident following challenge with the viral mimic, poly I:C (double stranded RNA), have been proposed to be common mechanisms leading to chronic fatigue and sickness [ 88 , 89 ]. Interestingly, pesticide exposure has likewise been implicated in multiple chemical sensitivity syndromes and general sickness symptoms [ 90 , 91 ].…”

Section: Discussionmentioning

confidence: 99%

An in vivo animal study assessing long-term changes in hypothalamic cytokines following perinatal exposure to a chemical mixture based on Arctic maternal body burden

et al. 2011

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BackgroundThe geographic distribution of environmental toxins is generally not uniform, with certain northern regions showing a particularly high concentration of pesticides, heavy metals and persistent organic pollutants. For instance, Northern Canadians are exposed to high levels of persistent organic pollutants like polychlorinated biphenyls (PCB), organochlorine pesticides (OCs) and methylmercury (MeHg), primarily through country foods. Previous studies have reported associations between neuronal pathology and exposure to such toxins. The present investigation assessed whether perinatal exposure (gestation and lactation) of rats to a chemical mixture (27 constituents comprised of PCBs, OCs and MeHg) based on Arctic maternal exposure profiles at concentrations near human exposure levels, would affect brain levels of several inflammatory cytokinesMethodsRats were dosed during gestation and lactation and cytokine levels were measured in the brains of offspring at five months of age. Hypothalamic cytokine protein levels were measured with a suspension-based array system and differences were determined using ANOVA and post hoc statistical tests.ResultsThe early life PCB treatment alone significantly elevated hypothalamic interleukin-6 (IL-6) levels in rats at five months of age to a degree comparable to that of the entire chemical mixture. Similarly, the full mixture (and to a lesser degree PCBs alone) elevated levels of the pro-inflammatory cytokine, IL-1b, as well as the anti-inflammatory cytokine, IL-10. The full mixture of chemicals also moderately increased (in an additive fashion) hypothalamic levels of the pro-inflammatory cytokines, IL-12 and tumor necrosis factor (TNF-α). Challenge with bacterial endotoxin at adulthood generally increased hypothalamic levels to such a degree that differences between the perinatally treated chemical groups were no longer detectable.ConclusionsThese data suggest that exposure at critical neurodevelopmental times to environmental chemicals at concentrations and combinations reflective of those observed in vulnerable population can have enduring consequences upon cytokines that are thought to contribute to a range of pathological states. In particular, such protracted alterations in the cytokine balance within the hypothalamus would be expected to favor marked changes in neuro-immune and hormonal communication that could have profound behavioral consequences.

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“…Consequently, this can result in increased expression of glucocorticoid receptors by a variety of immune cells, which can bind to and become activated by systemic cortisol/corticosterone. 18 Therefore, it has been suggested that markers of HPA axis functioning might serve as an indicator of chronic overreaction of the body’s stress system. 19 The stress caused by endometriosis symptoms has been hypothesized to cause a deregulation in the neuroendocrine–immune axis leading to disease.…”

Section: Introductionmentioning

confidence: 99%

Stress Exacerbates Endometriosis Manifestations and Inflammatory Parameters in an Animal Model

et al. 2012

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Women with endometriosis have significant emotional distress; however, the contribution of stress to the pathophysiology of this disease is unclear. We used a rat model of endometriosis to examine the effects of stress on the development of this condition and its influence on inflammatory parameters. Female Sprague-Dawley rats were subjected to swim stress for 10 consecutive days prior to the surgical induction of endometriosis by suturing uterine horn implants next to the intestinal mesentery (endo-stress). Sham-stress animals had sutures only, and an endo-no stress group was not subjected to the stress protocol. At the time of sacrifice on day 60, endometriotic vesicles were measured and colons assessed for macroscopic and microscopic damage. Colonic tissue and peritoneal fluid were collected for inflammatory cell analysis. Endometriosis, regardless of stress, produced a decrease in central corticotropin-releasing factor immunoreactivity, specifically in the CA3 subregion of the hippocampus. Prior exposure to stress increased both the number and severity of vesicles found in animals with endometriosis. Stress also increased colonic inflammation, motility, myeloperoxidase levels, and numbers of mast cells. In summary, prior stress may contribute to the development and severity of endometriosis in this animal model through mechanisms involving cell recruitment (eg, mast cells), release of inflammatory mediators, and deregulation of hypothalamic-pituitary axis responses in the hippocampus.

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Cellular and Molecular Mechanisms of the Interaction between the Immune and Neuroendocrine Systems in Experimental Chronic Fatigue Syndrome

Cited by 4 publications

References 19 publications

Bidirectional Crosstalk between Stress-Induced Gastric Ulcer and Depression under Chronic Stress

Bidirectional Crosstalk between Stress-Induced Gastric Ulcer and Depression under Chronic Stress

An in vivo animal study assessing long-term changes in hypothalamic cytokines following perinatal exposure to a chemical mixture based on Arctic maternal body burden

Stress Exacerbates Endometriosis Manifestations and Inflammatory Parameters in an Animal Model

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