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Published on: October 24, 2018
Cell-mediated immunity and its glucocorticoid-sensitivity after clinical recovery from severe major depressive
N Wodarz1, R Rupprecht, J Kornhuber
1Department of Psychiatry, University of Würzburg, FRG.
Insights
Following recovery from major depression, lymphocyte function and sensitivity to glucocorticoids normalize. This suggests reduced glucocorticoid receptor sensitivity is specific to the acute phase of depression.
Area of Science:
- Immunology
- Neuroendocrinology
- Psychiatry
Background:
- Major depression is associated with neuroendocrine alterations, including hypothalamic-pituitary-adrenal (HPA) axis dysregulation.
- Previous studies suggest impaired immune cell function and glucocorticoid sensitivity during acute depressive episodes.
Purpose of the Study:
- To investigate lymphocyte blastogenesis and in vitro dexamethasone sensitivity in patients recovered from severe major depression.
- To determine if immune cell function and glucocorticoid sensitivity remain altered after clinical remission of depression.
Main Methods:
- Assessed lymphocyte blastogenesis induced by concanavalin A, phytohemagglutinin A, and pokeweed mitogen in 12 recovered patients.
- Measured sensitivity to in vitro dexamethasone administration.
- Correlated immune responses with in vivo cortisol levels and clinical factors.
Main Results:
- Mitogen-driven lymphocyte proliferative responses were unchanged in recovered patients compared to baseline assessments during illness.
- No impairment of in vitro glucocorticoid sensitivity was observed in clinically recovered individuals.
- Inhibitory potency of dexamethasone was inversely correlated with in vivo adrenal cortical hormone levels.
Conclusions:
- Reduced glucocorticoid receptor sensitivity appears to be a transient phenomenon, occurring primarily during the acute phase of major depression.
- Immune function and glucocorticoid sensitivity normalize upon clinical recovery from severe depression.
Abstract:
This follow-up study investigated lymphocyte blastogenesis induced by concanavalin A, phytohemagglutinin A, and pokeweed mitogen and their sensitivity to in vitro dexamethasone administration in 12 patients clinically recovered from severe major depression. Although cortisol-levels at 4.00 p.m. decreased significantly after clinical remission, mitogen-driven lymphocyte proliferative responses were unchanged when assessed intra-individually. No impairment of in vitro glucocorticoid-sensitivity of lectin-induced lymphocyte blastogenesis could be observed in clinically recovered patients. The inhibitory potency of in vitro dexamethasone was found to be inversely correlated with in vivo adrenal cortical hormone levels. There were no correlations with age, weight, sex, antidepressant medication, severity or duration of depression. No differences from age- and sex-matched healthy individuals were found. These results indicate that reduced glucocorticoid receptor sensitivity occurs only during the acute depressive illness.
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