Disturbed neuroendocrine-immune interactions in chronic fatigue syndrome

The present study was designed to investigate the interaction between neuro endocrine mediators and the immune system in chronic fatigue syndrome (CFS) . Ne examined the sensitivity of the immune system to the glucocorticoid ag onist dexamethasone and the beta 2-adrenergic agonist terbutaline in 15 ado lescent girls with CFS and 14 age- and sex-matched controls. Dexamethasone inhibits T-cell proliferation in healthy controls and in CFS patients. Howe ver, the maximal effect of dexamethasone on T-cell proliferation is signifi cantly reduced in CFS patients as compared with controls. The beta 2-adrene rgic receptor agonist terbutaline inhibits tumor necrosis factor-a producti on and enhances interleukin-10 production by monocytes. Our data demonstrat e that the capacity of a beta 2-adrenergic agonist to regulate the producti on of these two cytokines is also reduced in CFS patients. We did not obser ve differences in baseline or CRH-induced cortisol and ACTH between CFS pat ients and controls. Baseline noradrenaline was similar in CFS and controls, whereas baseline adrenaline levels mere significantly higher in CFS patien ts. Ne conclude that CFS is accompanied by a relative resistance of the imm une system to regulation by the neuoendocrine system. Based on these data, me suggest CFS should be viewed as a disease of deficient neuroendocrine-im mune communication.