Psychosocial stress and liver disease status

Vere, Cristin Constantin; Streba, Costin Teodor; Streba, Letitia Maria; Ionescu, Alin Gabriel; Sima, Félix

doi:10.3748/wjg.15.2980

Cited by 62 publications

(45 citation statements)

References 79 publications

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“…The neuroimmunoendocrine regulation of PrP C in neutrophils and its impact upon the cytotoxic potential of this cell may help explain previous observations that behavioral stress, which modifies both the risk and the course of various diseases (51)(52)(53)(54)(55) and strongly modulates the immune system (56 -58), also affects the cytotoxic functions of neutrophils (59). Notably, the cytotoxicity of neutrophils often swings toward the production of tissue damage (15,16).…”

Section: Discussionmentioning

confidence: 78%

Neuroimmunoendocrine Regulation of the Prion Protein in Neutrophils

Mariante

Nóbrega

Martins

et al. 2012

Journal of Biological Chemistry

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Background: Prion protein (PrP C ) modulates inflammation, and prion diseases affect neutrophil numbers and functions, but the regulation of PrP C in neutrophils is unknown. Results: Inflammation and stress massively up-regulated PrP C in neutrophils via glucocorticoids and TGF-␤. Conclusion:We show a novel pathway of regulation of PrP C , with functional consequences for neutrophils. Significance: Systemic control of the expression and function of PrP C broadly modulates cellular physiology and pathology.The prion protein (PrP C ) is a cell surface protein expressed mainly in the nervous system. In addition to the role of its abnormal conformer in transmissible spongiform encephalopathies, normal PrP C may be implicated in other degenerative conditions often associated with inflammation. PrP C is also present in cells of hematopoietic origin, including T cells, dendritic cells, and macrophages, and it has been shown to modulate their functions. Here, we investigated the impact of inflammation and stress on the expression and function of PrP C in neutrophils, a cell type critically involved in both acute and chronic inflammation. We found that systemic injection of LPS induced transcription and translation of PrP C in mouse neutrophils. Up-regulation of PrP C was dependent on the serum content of TGF-␤ and glucocorticoids (GC), which, in turn, are contingent on the activation of the hypothalamic-pituitary-adrenal axis in response to systemic inflammation. GC and TGF-␤, either alone or in combination, directly up-regulated PrP C in neutrophils, and accordingly, the blockade of GC receptors in vivo curtailed the LPS-induced increase in the content of PrP C . Moreover, GC also mediated up-regulation of PrP C in neutrophils following noninflammatory restraint stress. Finally, neutrophils with upregulated PrP C presented enhanced peroxide-dependent cytotoxicity to endothelial cells. The data demonstrate a novel interplay of the nervous, endocrine, and immune systems upon both the expression and function of PrP C in neutrophils, which may have a broad impact upon the physiology and pathology of various organs and systems.

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Section: Discussionmentioning

confidence: 78%

Neuroimmunoendocrine Regulation of the Prion Protein in Neutrophils

Mariante

Nóbrega

Martins

et al. 2012

Journal of Biological Chemistry

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“…Adachi et al, via the same animal models, documented the development of oxidative damages to the DNA of hepatocytes after a period of 4 days of exposure (68). With regard to human studies, the understanding of the role played by stress on the onset and progression of acute and chronic liver diseases has assumed considerable importance in the current literature (42). In a recent review concerning the main scientific investigations carried out on the subject, Chida et al concluded that psychological stress promotes the development of a liver inflammatory response that can contribute (as a cause or contributory cause) to the risk of developing and/or worsening the course of various liver diseases (41).…”

Section: Comparing the Results Of The Questionnaire Hse And Liver Parmentioning

confidence: 99%

“…These preliminary studies, pointed out how under conditions of increased stress a physiological alteration of liver functions can be observed (40) and current scientific evidence confirms that psychosocial stress may both induce primitive liver injury and induce worsening of a pre-existing liver disease (41). The understanding of the effects of stress on the onset and progression of acute and chronic liver diseases has assumed considerable importance (42) and recent studies on animals and clinical evidences in humans are trying to clarify this complex relationship (43)(44)(45). These studies were carried out in a national and international context (40,41,(43)(44)(45) but the hepatic effects of specific exposures such as those related to chronic work stress were evaluated in very few epidemiological studies (46) and the bibliographic database on the topic is seriously incomplete.…”

Section: Stress and Stress Related Diseasesmentioning

confidence: 99%

Perceived stress and hepatic parameters

Tomei¹

2016

PER

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Introduction: the aim of the study is to evaluate work-related subjective stress in a group of employees, of both sexes, operating in the healthcare and welfare, through the administration of a questionnaire (HSE "Indicator Tool"), specifically developed and officially validated, and to analyze any possible correlations between stress levels taken from the questionnaire scores and the concentrations of three main hepatic parameters (GOT, GPT, GGT). Materials and methods: we studied a final sample of 232 subjects (143 males and 89 females) operating in the health and welfare sector. For research purposes during the medical examination each subject underwent the HSE indicator tool, a collection of information about relevant clinical and medical history and a venous blood sample for the assay of GOT, GPT and GGT. All questionnaires were analyzed using special software provided by the HSE. The results obtained from the questionnaires were statistically compared with the blood concentrations of hepatic parameters. Results: the dimensions found to be critical, associated with a stressful condition (yellow area) or a highly stressful condition (red area), are: managers support, colleagues support, quality of relationships and changes. The Pearson's correlation showed a statistically significant negative correlation (p <0.05) between the mean values of all the critical dimensions and the concentrations of the hepatic parameters, both on the total sample and after subdivision by gender. These results were confirmed in the multiple linear regression analysis, which indicated that the critical dimensions are the main significant variables contributing to the liver parameters alterations. Discussion: preliminary results indicate that a critical perception of stress at work can be statistically associated with increases in mean concentrations of GOT, GPT and GGT in a working asymptomatic population. These results provide a starting point for future studies on this topic, to a greater definition of the link between stress and liver injury, to confirm the effects on the parameters of liver injury (GOT, GPT, GGT) and to investigate possible correlations with the cholestasis parameters (bilirubin, alkaline phosphatase) and serum albumin.

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“…In recent years, the role of stress mediators in the liver pathophysiology has gained a new dimension [8, 10, 11]. Deviant increase in glucocorticoids following stress-arousal influences both food consumption and energy expenditure [12, 13].…”

Section: Introductionmentioning

confidence: 99%

Psychosocial-Stress, Liver Regeneration and Weight Gain: a Conspicuous Pathophysiological Triad

Ishtiaq

Khan

Arshad

2018

Cell Physiol Biochem

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Psychosocial stress alters several physiological parameters resulting in multiple disorders, particularly compromising the immune system thereby provoking various diseases including liver disorders. However, the plausible underlying mechanisms remain elusive. Recent literature provides mechanistic evidences of detrimental effects of psychosocial stress on physiology of different body organs including liver. The data of stress-induced pathophysiological changes in liver functions and obesity were systematically collected from PubMed, ScienceDirect and the Web of Science Databases published in English. Stress and glucocorticoids (GCs) control food intake and energy expenditure through appetite stimulators neuropeptide Y (NYP) and agouti-related protein (AgRP) in hypothalamus. Principle effectors of the activated hypothalamic-pituitary-adrenal (HPA) axis in response to psychosocial stress are proopiomelanocortin (POMC)-derived adrenocorticotropic hormone (ACTH) and GCs. Stress-induced GCs hyper-secretion triggers glucocorticoid receptor (GR)-dependent transcriptional factor, nuclear factor kappa B (NFκB), which interferes TNFα-IL6 and keap1-Nrf2 pathways in liver regeneration and obesity through fine-tuning of TNFα, IL6 and Nrf2 signaling. In this review, it is contrived upon existing evidence to put forward a model whereby exposure to life-stress has a prominent impact over weight gain and can alter the regenerative mode of a damaged liver through Keap1-Nrf2 and TNFa-IL6 pathways.

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Psychosocial stress and liver disease status

Cited by 62 publications

References 79 publications

Neuroimmunoendocrine Regulation of the Prion Protein in Neutrophils

Neuroimmunoendocrine Regulation of the Prion Protein in Neutrophils

Perceived stress and hepatic parameters

Psychosocial-Stress, Liver Regeneration and Weight Gain: a Conspicuous Pathophysiological Triad

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