Insufficient glucocorticoid signaling and elevated inflammation in coronary heart disease patients with comorbid depression
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Coronary heart disease (CHD) and depression are very common and often co-existing disorders. In addition to psychological and social morbidity, depression exacerbates adverse cardiac outcomes in CHD patients. Inflammation has been proposed as one of the mechanisms involved in the association between these two debilitating diseases. Therefore, the present study aimed to evaluate inflammatory responses as well as to investigate the pathophysiological mechanisms underlying the putative inflammatory activation in CHD patients with and without depression, by assessing the function of two important biological factors regulating inflammation, the hypothalamus-pituitary-adrenal (HPA) axis and the glucocorticoid receptor (GR). Eighty-three CHD patients with (n=28) and without (n=55) comorbid depression were recruited from primary care services in South London. Depression status was assessed by means of Clinical Interview Schedule Revised for diagnosis of depression, and Beck Depression Inventory for the presence of depressive symptoms. Serum C-reactive protein (CRP), plasma vascular endothelial growth factor (VEGF), and plasma and salivary cortisol were measured using commercially available ELISA kits. Gene expression of GR and interleukin-6 (IL-6) were conducted via qPCR. GR sensitivity was evaluated in vitro in isolated peripheral blood mononuclear cells using the dexamethasone inhibition of lipopolysaccharide-stimulated IL-6 levels. Serum levels of kynurenine pathway metabolites were measured using high performance liquid chromatography. Our results show that CHD patients with depression had higher levels of CRP, IL-6 gene expression, and VEGF compared with CHD non-depressed, as well as lower plasma and saliva cortisol levels. The CHD depressed group also exhibited a reduction in GR expression and sensitivity. Finally, tryptophan levels were significantly lower in patients with depression, who also showed an increased kynurenine/tryptophan ratio. In conclusion, CHD patients with depression had elevated levels of inflammation in the context of HPA axis hypoactivity, GR resistance, and increased activation of the kynurenine pathway. Reduced cortisol bioavailability and attenuated glucocorticoid responsiveness due to decreased expression and sensitivity of GR may lead to insufficient glucocorticoid signaling and thus elevation of inflammation in these patients.
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In depressed patients with coronary heart disease, these findings were not associated with HPA axis hyperactivity but rather with hypoactivity.
“these findings were not associated with HPA axis hyperactivity but rather with hypoactivity.”
From Why are depressed patients inflamed? A reflection on 20 years of research on depression, glucocorticoid resistance and inflammation (2017) · cites this paper as Nikkheslat et al., 2015
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Pariante, C. M. (2017) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2017.04.001 · Cited by 382 · see citing works
Self-citationKynurenine pathway in depression: a systematic review and meta-analysis
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The role of depressive subtypes within the neuroinflammation hypothesis of major depressive disorder
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Longitudinal associations between glucocorticoid receptor methylation and late-life depression
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- Authors
- Nikkheslat, N., Zunszain, P. A., Horowitz, M. A., Barbosa, I. G., Parker, J. A., Myint, A.-M., Schwarz, M. J., Tylee, A. T., Carvalho, L. A., & Pariante, C. M.
- Affiliations
- King's College London (GB)
- University of Roehampton (GB)
- Ludwig-Maximilians-Universität München (DE)
- University College London (GB)
- Corresponding author
- Pariante, Carmine M.
- ORCID
- Venue
- Brain Behavior and Immunity
- Publisher
- Elsevier BV
- Published
- 2015-08
- Volume
- 48
- Pages
- 8-18
- ISSN
- 0889-1591 (ISSN-L)
- OpenAlex
- W2092017894
- Cited by
- 147
- References
- 117
- Citations by year
- 2026: 7 · 2025: 12 · 2024: 8 · 2023: 14 · 2022: 14 · 2021: 9 · 2020: 14 · 2019: 12 · 2018: 27 · 2017: 11 · 2016: 10 · 2015: 9
- FWCI
- 9.90
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Brain Behavior and Immunity (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion, cc-by-nc-nd)
- Funders
- NIHR (National Institute for Health Research) Biomedical Research Centre (BRC) and Dementia Unit at South London
- Maudsley NHS (National Health Service) Foundation Trust and King’s College London
- BHF (British Heart Foundation)
- ECNP (European College of Neuropsychopharmacology)
- NARSAD (National Association for Research on Schizophrenia and Affective Disorders) Young Investigator Awards
- NIHR Programme Grants
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Health and Mental Health
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- coronary artery disease, depression, comorbidities, inflammation, glucocorticoid signaling, glucocorticoid receptor, cortisol, C-reactive protein, interleukin-6, vascular endothelial growth factor, kynurenine pathway, tryptophan metabolism, glucocorticoid resistance
- MeSH terms
- Age Factors, Aged, C-Reactive Protein, Coronary Disease, Depressive Disorder, Female, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Leukocytes, Mononuclear, Male, Pituitary-Adrenal System, Psychiatric Status Rating Scales, Receptors, Glucocorticoid, Sex Factors, Signal Transduction, Biomarkers, Interleukin-6, Vascular Endothelial Growth Factor A
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