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Published on: September 29, 2021
Immune and endocrine function in burnout syndrome
Paula M C Mommersteeg1, Cobi J Heijnen, Annemieke Kavelaars
1Department of Health Psychology, Utrecht University, Utrecht, The Netherlands.
Psychosomatic Medicine
|November 3, 2006
Summary
Individuals with burnout syndrome exhibit increased production of the anti-inflammatory cytokine interleukin-10 (IL-10) by monocytes. This immune response in burnout does not appear to be influenced by glucocorticoids or altered glucocorticoid receptor function.
Area of Science:
- Immunology
- Endocrinology
- Occupational Health
Background:
- Burnout is a stress-related syndrome linked to increased infection risk, suggesting immune system compromise.
- Understanding the endocrine and immune dysfunctions in burnout is crucial for effective management.
Purpose of the Study:
- To investigate endocrine and ex vivo immune function in individuals with severe burnout.
- To compare immune cell profiles and cytokine release in burnout patients versus healthy controls.
Main Methods:
- Compared endocrine (cortisol, DHEAS) and immune (T, B, NK cells, cytokine release) variables in 56 burnout patients and 38 controls.
- Assessed in vitro cytokine production (IL-10, IFN-γ, TNF-α) and dexamethasone's regulatory capacity.
- Analyzed salivary cortisol and DHEAS levels.
Main Results:
- Burnout group showed increased monocyte production of anti-inflammatory interleukin-10 (IL-10) after lipopolysaccharide stimulation.
- No significant differences in pro-inflammatory cytokines (IFN-γ, TNF-α) or T, B, NK cell counts were observed.
- Higher dehydroepiandrosterone-sulphate (DHEAS) levels were found in the burnout group, but cortisol levels and dexamethasone's regulatory capacity did not differ.
Conclusions:
- Monocyte production of IL-10 is elevated in burnout syndrome.
- Glucocorticoids or altered glucocorticoid receptor function are unlikely to drive the increased IL-10 production in burnout.
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