Immune and endocrine function in burnout syndrome

Objective: Burnout is a stress-induced work-related syndrome. It is associated with a higher incidence of infections possibly pointing to a compromised immune system. In the present study, endocrine and ex vivo immune function of severe cases of burnout were investigated. Methods: Endocrine and immune variables were compared in 56 persons with burnout and 38 healthy control subjects. Cortisol after awakening, after a low-dose dexamethasone, and dehydroepiandrosterone-sulphate (DHEAS) were analyzed from saliva. Peripheral blood was analyzed for T, B, and NK cell number and in vitro mitogen-induced pro- and antiinflammatory cytokine release. The capacity of dexamethasone to regulate cytokine release was compared between the groups. Results: The burnout group showed an increased production of the antiinflammatory cytokine interleukin-10 (IL-10) by monocytes after lipopolysaccharide stimulation. No differences were observed in IL-10 release induced by the T-cell mitogen PHA nor in the proinflammatory cytokines gamma interferon and tumor necrosis factor alpha. The capacity of dexamethasone to regulate cytokine release did not differ between the groups. The number of peripheral blood T cells, B cells, or NK cells was not different either. The burnout group showed higher DHEAS levels but no difference in cortisol levels after awakening or after dexamethasone intake in comparison to controls. Conclusion: Production of the antiinflammatory cytokine IL-10 by monocytes was increased in individuals with burnout syndrome. It seems unlikely that glucocorticoids or changes in glucocorticoid receptor function play a role in this higher IL-10 production.