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Cited by 75Stress Responses and CortisolAdipokines, Inflammation, and Metabolic DiseasesSleep and Work-Related Fatigue

Reduced Glucocorticoid Sensitivity of Monocyte Interleukin-6 Production in Male Industrial Employees who are Vitally Exhausted

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Wirtz, Petra H., Von KÄnel, Roland, Schnorpfeil, Pia, Ehlert, Ulrike, Frey, Karl, Fischer, Joachim E.·2003·Psychosomatic Medicine
DOI 10.1097/01.psy.0000062529.39901.c7
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Abstract

OBJECTIVE: Proinflammatory changes are thought to link vital exhaustion with adverse cardiovascular outcomes. Monocytes play a central role in the pathogenesis of atherosclerotic lesions and are a major source of circulating cytokines. We hypothesized that vital exhaustion may alter the regulation of monocyte activity, as measured by lipopolysaccharide (LPS)-stimulated and glucocorticoid inhibited release of the proinflammatory cytokine interleukin-6 (IL-6). METHODS: In 166 middle-aged apparently healthy men, vital exhaustion was measured by the Shortened Maastricht Exhaustion Questionnaire. Subjects in the highest quartile (highly exhausted, N= 38) were compared with those in the second and third quartiles (moderately exhausted N= 89) vs. those in the lowest quartile (nonexhausted, N= 39) in terms of plasma C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-alpha) levels, and as to IL-6 release after LPS stimulation in vitro. Inhibition of IL-6 release was determined by coincubation with increasing concentrations of dexamethasone. Monocyte glucocorticoid sensitivity was defined as the dexamethasone concentration inhibiting IL-6 release by 50%. RESULTS: Highly exhausted individuals had higher CRP levels than nonexhausted subjects (p=.008). LPS-stimulated IL-6 release was not significantly different between groups. However, in highly exhausted participants, dexamethasone was less able to inhibit IL-6 release (p=.010), and the glucocorticoid sensitivity was lower (p=.003) than in nonexhausted subjects. CONCLUSIONS: In highly exhausted individuals, glucocorticoids exert less suppressive action on monocyte IL-6 release than in nonexhausted subjects. This finding points to altered regulation of monocyte cytokine production as one possible pathway linking exhaustion with atherosclerosis.

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  • Chronic stressors have been shown to diminish the capacity of glucocorticoids to suppress endotoxin-stimulated cytokine production in humans and animals.

    “Support for this account has accrued in studies of humans and animals (14,17,19,20), where chronic stressors have been shown to diminish the capacity of glucocorticoids to suppress endotoxin-stimulated cytokine production.”

    From A Functional Genomic Fingerprint of Chronic Stress in Humans: Blunted Glucocorticoid and Increased NF-κB Signaling (2008) · cites this paper as [20]

    The Results (Inhibition of Stimulated Cytokine Production; page not provided) report that dexamethasone was less able to inhibit LPS-stimulated IL-6 release in highly exhausted men than in nonexhausted men. The paper supports an association in this human group, but it does not study animals or establish that chronic stressors caused the reduced sensitivity. (LLM, conf=0.88)

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  • Initial support for the proposition that chronic stressors bring about functional resistance to cortisol-mediated signaling has emerged in studies showing chronic stressors diminish the capacity of glucocorticoids to suppress ex vivo inflammatory cytokine production.

    “Initial support for this proposition has emerged in a series of studies where chronic stressors have been shown to diminish the capacity of glucocorticoids to suppress ex vivo inflammatory cytokine production (14,17,19,20).”

    From A Functional Genomic Fingerprint of Chronic Stress in Humans: Blunted Glucocorticoid and Increased NF-κB Signaling (2008) · cites this paper as [20]

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  • Prolonged hyperactivity of the HPA-axis could result in blunted anti-inflammatory responses to glucocorticoids, resulting in increased inflammation.

    “prolonged hyperactivity of the hypothalamus–pituitary–adrenal-axis could result in blunted anti-inflammatory responses to glucocorticoids resulting in increased inflammation.35, 36”

    From Association of depressive disorders, depression characteristics and antidepressant medication with inflammation (2012) · cites this paper as [36]

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Research works printed but not linked: 1

  1. Cole SR, Kawachi I, Sesso HD, Paffenbarger RS, Lee IM. Sense of exhaustion and coronary heart disease among college alumni. Am J Cardiol 1999;84:1401-1405.

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Authors
Wirtz, P. H., Von KÄnel, R., Schnorpfeil, P., Ehlert, U., Frey, K., & Fischer, J. E.
Affiliations
  • ETH Zurich (CH)
  • University of Zurich (CH)
ORCID
Venue
Psychosomatic Medicine
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2003-07
Volume
65
Issue
4
Pages
672-678
ISSN
0033-3174 (ISSN-L)
DOI
10.1097/01.psy.0000062529.39901.c7
OpenAlex
W2002409458
Cited by
75
References
45
Citations by year
2025: 1 · 2024: 2 · 2023: 1 · 2022: 4 · 2021: 1 · 2020: 1 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 1 · 2014: 3 · 2013: 6 · 2012: 6
FWCI
1.89
Type
journal article
Language
en
Open access
Locations
  • Psychosomatic Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • KOPS (University of Konstanz) (submittedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
Keywords
vital exhaustion, glucocorticoid sensitivity, monocytes, interleukin-6, dexamethasone, lipopolysaccharide stimulation, C-reactive protein, TNF-α, inflammatory cytokines, atherosclerosis, cardiovascular risk, occupational stress, industrial workers
MeSH terms
Adult, Arteriosclerosis, C-Reactive Protein, Dexamethasone, Employment, Fatigue, Gene Expression Regulation, Humans, Industry, Inflammation, Lipopolysaccharides, Male, Middle Aged, Monocytes, Severity of Illness Index, Switzerland, Tumor Necrosis Factor-alpha, Interleukin-6

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