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Cited by 253Stress Responses and CortisolTryptophan and brain disordersCancer, Stress, Anesthesia, and Immune Response

Clinical depression and regulation of the inflammatory response during acute stress

Miller, Gregory E., Rohleder, Nicolas, Stetler, Cinnamon, Kirschbaum, Clemens·2005·Psychosomatic Medicine
DOI 10.1097/01.psy.0000174172.82428.ce
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Abstract

OBJECTIVE: This study examined whether clinical depression is associated with a differential inflammatory response to an acute bout of psychological stress. METHODS: A total of 72 women participated in the study; half met diagnostic criteria for clinical depression; the others had no history of psychiatric illness. The groups were matched with respect to age and ethnicity. All subjects were exposed to a 17-minute mock-job interview; blood was drawn to assess secretion and regulation of inflammatory molecules. RESULTS: The stressor was associated with feelings of shame and anxiety, a mobilization of monocytes, neutrophils, and C-reactive protein into the circulation, and greater endotoxin-stimulated production of interleukin-6 and tumor necrosis factor-alpha by white blood cells in vitro. Depressed subjects began the session with greater sensitivity to the antiinflammatory properties of glucocorticoids than control subjects. Following exposure to the stressor protocol, however, sensitivity decreased among depressed subjects and increased among controls. This was manifest by disparities in interleukin-6 and tumor necrosis factor-alpha production in the presence of dexamethasone. CONCLUSIONS: These findings suggest that under acutely challenging conditions, depression is associated with greater resistance to molecules that normally terminate the inflammatory cascade. An impaired capacity to regulate inflammation could underlie some of the excess morbidity and mortality that has been associated with depression.

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Crossref · 10.1097/01.psy.0000174172.82428.ce

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69 of 69 references verified0 citation errors · 0 not checkable

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  • Compared to nondepressed women, depressed women exhibited elevations in CRP that persisted following the TSST.

    “Compared to nondepressed women, however, depressed women exhibited elevations in CRP that persisted following the TSST”

    From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as G. E. Miller et al., 2005

  • In depressed and nondepressed women exposed to a TSST variant, the experience evoked increases in anxiety and shame and greater LPS-stimulated production of TNFα and IL-6 for both groups.

    “This experience evoked increases in anxiety and shame and greater LPS-stimulated production of TNFα and IL-6 for both depressed and nondepressed women.”

    From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as G. E. Miller, Rohleder, Stetler, and Kirschbaum (2005)

  • Following stressor administration, depressed patients became significantly less sensitive to DEX in vitro, whereas controls became significantly more sensitive.

    “following stressor administration, depressed patients became significantly less sensitive to DEX in vitro, whereas controls became significantly more sensitive.87”

    From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [87]

  • Increased in vitro sensitivity of innate immune responses to glucocorticoids was found in depressed patients prior to a laboratory stressor.

    “Increased in vitro sensitivity of innate immune responses to glucocorticoids was also found in depressed patients prior to a laboratory stressor”

    From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [87]

  • Resistance to glucocorticoids and mild systemic inflammation have been implicated in the pathogenesis of depression, suggesting that the dynamics observed may help explain affective difficulties among caregivers.

    “Notably, resistance to glucocorticoids and mild, systemic inflammation have also been implicated in the pathogenesis of depression (15,40–42), suggesting that the dynamics observed herein may help explain the affective difficulties often found among caregivers (43).”

    From A Functional Genomic Fingerprint of Chronic Stress in Humans: Blunted Glucocorticoid and Increased NF-κB Signaling (2008) · cites this paper as [40]

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Authors
Miller, G. E., Rohleder, N., Stetler, C., & Kirschbaum, C.
Affiliations
University of British Columbia (CA)
Corresponding author
Miller, Gregory E.
ORCID
Venue
Psychosomatic Medicine
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2005-09
Volume
67
Issue
5
Pages
679-687
ISSN
0033-3174 (ISSN-L)
DOI
10.1097/01.psy.0000174172.82428.ce
OpenAlex
W2162870899
Cited by
253
References
69
Citations by year
2026: 1 · 2025: 7 · 2024: 8 · 2023: 6 · 2022: 7 · 2021: 12 · 2020: 8 · 2019: 15 · 2018: 8 · 2017: 14 · 2016: 10 · 2015: 9 · 2014: 21 · 2013: 14 · 2012: 17
FWCI
6.01
Type
journal article
Language
en
Open access
closed
Locations
  • Psychosomatic Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
Keywords
major depressive disorder, inflammation, acute psychological stress, C-reactive protein, interleukin-6, TNF-α, glucocorticoid sensitivity, dexamethasone, monocytes, neutrophils, endotoxin, mock job interviews, women
MeSH terms
Acute Disease, Adult, C-Reactive Protein, Major Depressive Disorder, Endotoxins, Female, Glucocorticoids, Humans, Hydrocortisone, Inflammation, Monocytes, Stress, Psychological, Tumor Necrosis Factor-alpha, Interleukin-6, Cytokines, In Vitro Techniques

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