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Chronic psychological stress and the regulation of pro-inflammatory cytokines: A glucocorticoid-resistance model
Abstract
This study examined whether chronic stress impairs the immune system's capacity to respond to hormonal signals that terminate inflammation.Fifty healthy adults were studied; half were parents of cancer patients, and half were parents of healthy children.Parents of cancer patients reported more psychological distress than parents of healthy children.They also had flatter diurnal slopes of cortisol secretion, primarily because of reduced output during the morning hours.There was also evidence that chronic stress impaired the immune system's response to anti-inflammatory signals: The capacity of a synthetic glucocorticoid hormone to suppress in vitro production of the pro-inflammatory cytokine interleukin-6 was diminished among parents of cancer patients.Findings suggest a novel pathway by which chronic stress might alter the course of inflammatory disease.
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These dysfunctions increase vulnerability to inflammatory or autoimmune diseases due to inadequate glucocorticoid-mediated immune regulation.
“Additionally, these dysfunctions increase the vulnerability to inflammatory or autoimmune diseases due to inadequate glucocorticoid-mediated immune regulation [21].”
From Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation (2025) · cites this paper as [21]
Over time, the initial state of hypercortisolism may evolve into other stages, including adrenal gland adaptive changes.
“Over time, the initial state of hypercortisolism may evolve into other stages: the extreme and persistent demand on the HPA axis present during chronic stress conditions may also lead to adrenal gland adaptive changes [11,21].”
From Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation (2025) · cites this paper as [21]
Among parents of cancer patients, dexamethasone's ability to suppress IL-6 production was significantly reduced compared to parents of medically healthy children.
“The results provided preliminary support: among parents of cancer patients, dexamethasone’s ability to suppress IL-6 production was significantly reduced compared to parents of medically healthy children [21].”
From Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation (2025) · cites this paper as [21]
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 [35]
Evidence for GCR in response to chronic stress has been found in parents of children with cancer, spouses of brain-cancer patients, and persons reporting high levels of loneliness.
“Evidence for GCR in response to chronic stress has been found in parents of children with cancer (10), spouses of brain-cancer patients (11) and in persons reporting high levels of loneliness (5).”
From Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk (2012) · cites this paper as [10]
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 [14]
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 [14]
Prolonged or chronic stress in humans can lead to glucocorticoid receptor insensitivity in immune cells.
“Similarly, prolonged or chronic stress in humans can lead to GR insensitivity, meaning that GRs in immune cells are not able to “hear” the inhibitory signals of glucocorticoids (Cohen et al., 2012; Miller et al., 2002).”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Miller et al., 2002
Continued exposure to high cortisol may eventually lead to glucocorticoid insensitivity.
“For instance, continued exposure to high cortisol may eventually lead to glucocorticoid insensitivity (Cohen et al., 2012; Miller et al., 2002)”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Miller et al., 2002
Caregiving for a child with cancer has been associated with diminished inhibition of LPS-stimulated IL-6 production following glucocorticoid administration.
“Caregiving for a child with cancer has been associated with diminished inhibition of LPS-stimulated IL-6 production following glucocorticoid administration”
From Close relationships, inflammation, and health (2010) · cites this paper as Miller et al., 2002
Diminished sensitivity to the anti-inflammatory properties of glucocorticoids provides one potential mechanism through which chronic interpersonal stressors such as caregiving promote chronic low grade inflammation.
“Diminished sensitivity to the anti-inflammatory properties of glucocorticoids provides one potential mechanism through which chronic interpersonal stressors such as caregiving promote chronic low grade inflammation.”
From Close relationships, inflammation, and health (2010) · cites this paper as Miller et al., 2002
Glucocorticoid resistance occurs when immune cells become less sensitive to the anti-inflammatory effects of glucocorticoids due to persistent or repeated HPA axis activation.
“occurs when immune cells become less sensitive to the anti-inflammatory effects of glucocorticoids as a consequence of persistent or repeated activation of the HPA axis”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Miller et al, 2002
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Self-citationA prospective population-based study of triggers of symptomatic flares in IBD
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“Preclinical research has shown GC resistance in immune cells following repeated acute stress (208, 209), while in humans, prolonged or chronic stress leads also to GR insensitivity of immune cells and, respectively, altered GC inhibitory signal (112, 210).”
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The impact of stress on the development and expression of atopy
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Social support, social integration, and inflammatory cytokines: a meta-analysis
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Psychological Stress and Mitochondria: A Conceptual Framework
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Giving Up on Unattainable Goals: Benefits for Health?
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Self-citationMoving to Beat Anxiety: Epidemiology and Therapeutic Issues with Physical Activity for Anxiety
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Clinical depression and regulation of the inflammatory response during acute stress
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Self-citationExtensive expertise in endocrinology: adrenal crisis
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Cognitive-Behavioral Stress Management Reverses Anxiety-Related Leukocyte Transcriptional Dynamics
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Social relationships, sleep quality, and interleukin-6 in aging women
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A Framework for Examining Social Stress and Susceptibility to Air Pollution in Respiratory Health
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Socioeconomic Status, Stress, and Immune Markers in Adolescents With Asthma
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Interleukin-6, Cortisol, and Depressive Symptoms in Ovarian Cancer Patients
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Affective reactivity to daily stressors is associated with elevated inflammation
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Neuroimmunological effects of physical exercise in depression
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Chronic stress, salivary cortisol, and α-amylase in children with asthma and healthy children
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Inflammatory cytokine-associated depression
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Do NSAIDs, Antibiotics, Infections, or Stress Trigger Flares in IBD?
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Self-citationStress-induced biological aging: A review and guide for research priorities
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Metadata
- Authors
- Miller, G. E., Cohen, S., & Ritchey, A. K.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Miller, Gregory E.
- Venue
- Health Psychology
- Published
- 2002
- Volume
- 21
- Issue
- 6
- Pages
- 531-541
- ISSN
- 0278-6133 (ISSN-L)
- 1930-7810
- OpenAlex
- W4242918118
- Cited by
- 769
- References
- 89
- Citations by year
- 2026: 38 · 2025: 24 · 2024: 35 · 2023: 26 · 2022: 38 · 2021: 43 · 2020: 35 · 2019: 45 · 2018: 43 · 2017: 25 · 2016: 42 · 2015: 40 · 2014: 34 · 2013: 32 · 2012: 50
- FWCI
- 4.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Health Psychology (publishedVersion)
- Funders
- American Heart Association
- National Heart, Lung, and Blood Institute (HL65111, HL65112)
- National Institute of Mental Health (MH 50430)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Stress, Anesthesia, and Immune Response
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- chronic psychological stress, inflammatory cytokines, interleukin-6, glucocorticoid resistance, diurnal cortisol rhythm, parents of cancer patients, psychological distress, inflammation, immune regulation
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