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Multiple reciprocal relationships between in vivo cellular immunity and hypothalamic–pituitary–adrenal axis in depression

Published online by Cambridge University Press:  09 July 2009

M. Maes ,
H. Y. Meltzer ,
W. Stevens ,
P. Cosyns  and
P. Blockx
M. Maes*
Affiliation:
Department of Psychiatry of the University Hospitals of Cleveland, Ohio, USA; Department of Psychiatry, Department of Immunology and Department of Nuclear Medicine, University Hospital, Antwerp, Belgium
H. Y. Meltzer
Affiliation:
Department of Psychiatry of the University Hospitals of Cleveland, Ohio, USA; Department of Psychiatry, Department of Immunology and Department of Nuclear Medicine, University Hospital, Antwerp, Belgium
W. Stevens
Affiliation:
Department of Psychiatry of the University Hospitals of Cleveland, Ohio, USA; Department of Psychiatry, Department of Immunology and Department of Nuclear Medicine, University Hospital, Antwerp, Belgium
P. Cosyns
Affiliation:
Department of Psychiatry of the University Hospitals of Cleveland, Ohio, USA; Department of Psychiatry, Department of Immunology and Department of Nuclear Medicine, University Hospital, Antwerp, Belgium
P. Blockx
Affiliation:
Department of Psychiatry of the University Hospitals of Cleveland, Ohio, USA; Department of Psychiatry, Department of Immunology and Department of Nuclear Medicine, University Hospital, Antwerp, Belgium
*
1Address for correspondence. Dr Michael Maes, Department of Psychiatry, University Hospitals of Cleveland, Hanna Pavilion, Room B-68, 2040 Abington Road, Cleveland, Ohio 44106, USA.
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Synopsis

Major depression is reportedly characterized by increased activity of the hypothalamic–pituitary–adrenal (HPA) axis and by in vivo immune activation. The present study was carried out in order to investigate the relationships between HPA-axis activity and in vivo immune function in depression. Towards this end the following parameters were measured: 24 h urinary cortisol (UC) excretion; basal and post-dexamethasone (DST) plasma cortisol, β-endorphin/β-lipotropin (βEND/βLPH) and dexamethasone concentrations; and leucocyte subsets (i.e. lymphocytes, neutrophils, monocytes, CD4+, CD4+CD45RA+, CD4+CD45RO+, CD8+, CD8+CD57+, CD8+CD57−, HLA-DR+, CD25+ T cells, HLA-DR+, CD19+, CD20+, and CD21+ B cells) both pre-and post-DST. Dexamethasone administration (1 mg orally) induced leucocytosis, lymphocytopaenia, monocytopaenia and neutrophilia. HPA-axis non-suppressors exhibited a relative resistance to the enhancing (e.g. neutrophils) or depressant (e.g. lymphocytes, CD4+ T cells) effects of dexamethasone. There were significant correlations between UC excretion and the number of percentage of lymphocytes, monocytes, CD4+CD45RA+ and CD8+CD57− T cells (negatively) and neutrophils (positively). It is concluded that multiple and complex intertwined relationships between HPA-axis hyperactivity and systemic immune stimulation participate in the pathophysiology or pathogenesis of major depression.

Type
Original Articles
Information
Psychological Medicine , Volume 24 , Issue 1 , February 1994 , pp. 167 - 177
Copyright
Copyright © Cambridge University Press 1994

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