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Altered glucocorticoid immunoregulation in treatment resistant depression
Moisés E Bauer1, Andrew Papadopoulos, Lucia Poon
1Department of Microbiological Sciences, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul, 90619-900 Porto Alegre, RS, Brazil. mebauer@pucrs.br
Psychoneuroendocrinology
|November 26, 2002
Summary
Treatment-resistant depression (TRD) is linked to altered immune cell function and steroid regulation. Lymphocyte resistance to glucocorticoids may be associated with TRD, not elevated cortisol levels.
Area of Science:
- Neuroimmunology
- Endocrinology
- Psychiatry
Background:
- Cellular immune function alterations are linked to depression and endocrine changes.
- The hypothalamic-pituitary-adrenal (HPA) axis and T-cell responses are implicated in depression.
Purpose of the Study:
- Assess HPA axis function in treatment-resistant depression (TRD).
- Evaluate T-cell proliferation and cytokine production in TRD.
- Determine lymphocyte sensitivity to glucocorticoids (GCs) in vitro.
Main Methods:
- Measured salivary cortisol hourly before and after dexamethasone (DEX) in 36 TRD patients and 31 controls.
- Classified patients into HPA axis suppressors and nonsuppressors.
- Assessed in vitro phytohemagglutinin-induced T-cell proliferation, cytokine production (IL-2, TNF-alpha), and lymphocyte sensitivity to cortisol and DEX.
Main Results:
- No difference in basal cortisol, T-cell proliferation, or cytokine production between patients and controls.
- Nonsuppressors had significantly higher post-DEX cortisol levels than suppressors.
- Nonsuppressors produced significantly less TNF-alpha.
- Lymphocyte proliferation and cytokine production were less suppressed by GCs in depressives compared to controls.
Conclusions:
- Altered immune function and steroid regulation in depression are not linked to elevated basal cortisol.
- Lymphocyte resistance to steroids may be associated with TRD.
- Further research into neuroimmune mechanisms in TRD is warranted.