Cited by 364Stress Responses and CortisolTryptophan and brain disordersTreatment of Major Depression

Interleukin-1 beta: a putative mediator of HPA axis hyperactivity in major depression?

Michael H. J. Maes, Eugène Bosmans, Herbert Y. Meltzer, Simon Scharpé, Eduard Suy·1993·American Journal of Psychiatry

Abstract

Objective There is extensive evidence that major depression, and particularly melancholia, is characterized by hypothalamic-pituitary-adrenal (HPA) axis hyperactivity as well as systemic immune activation, which may be accompanied by increased interleukin-1 beta production. Interleukin-1 beta is known to enhance HPA axis activity during an immune response. This study investigated whether interleukin-1 beta production is related to HPA axis activity in depressed subjects. Method The subjects were 28 inpatients with major or minor depression and 10 normal comparison subjects. The authors measured 1) the subjects' cortisol levels after an overnight 1-mg dexamethasone suppression test (DST) and 2) mitogen-stimulated supernatant interleukin-1 beta production by peripheral blood mononuclear cells. Results Statistically significant positive correlations between interleukin-1 beta production and post-DST cortisol values were found in the study group as a whole and in the depressed and normal subgroups separately. Conclusions It is suggested that constituents of the immune response (such as interleukin-1 beta) in major depression may contribute to HPA axis hyperfunction in that illness.

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Crossref · 10.1176/ajp.150.8.1189

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2 of 2 references verified0 citation errors · 0 not checkable

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  • One of the earliest studies showed a significant correlation between post-DEX concentrations of cortisol and the production of IL-1 by peripheral blood mononuclear cells.

    “one of the earliest studies in this regard showed a significant correlation between post-DEX concentrations of cortisol and the production of IL-1 by peripheral blood mononuclear cells.85”

    From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [85]

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Authors
Maes, M. H. J., Bosmans, E., Meltzer, H. Y., Scharpé, S., & Suy, E.
Affiliations
  • University Hospitals of Cleveland (US)
  • University of Antwerp (BE)
Venue
American Journal of Psychiatry
Published
1993-08-01
Volume
150
Issue
8
Pages
1189-1193
ISSN
  • 0002-953X (ISSN-L)
  • 1535-7228
OpenAlex
W33142977
Cited by
364
References
2
Citations by year
2026: 1 · 2025: 6 · 2024: 1 · 2023: 7 · 2022: 8 · 2021: 7 · 2020: 9 · 2019: 7 · 2018: 12 · 2017: 16 · 2016: 15 · 2015: 17 · 2014: 7 · 2013: 16 · 2012: 16
FWCI
4.57
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of Mental Health (NIMH MH-41684, NIMH MH-47808)
  • National Center for Research Resources (RR 00080)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Keywords
IL-1β, HPA axis hyperactivity, major depressive disorder, melancholia, cortisol, dexamethasone suppression test, peripheral blood mononuclear cells, immune activation, neuroendocrine-immune interaction
MeSH terms
Adult, Depressive Disorder, Dexamethasone, Hospitalization, Humans, Hydrocortisone, Interleukin-1, Lymphocyte Activation, Lymphocytes, Middle Aged

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