Disturbed Neuroendocrine-Immune Interactions in Chronic Fatigue Syndrome

The present study was designed to investigate the interaction between neuroendocrine mediators and the immune system in chronic fatigue syndrome (CFS). We examined the sensitivity of the immune system to the glucocorticoid agonist dexamethasone and the b2-adrenergic agonist terbutaline in 15 adolescent girls with CFS and 14 age- and sex-matched controls. Dexamethasone inhibits T-cell proliferation in healthy controls and in CFS patients. However, the maximal effect of dexamethasone on T-cell proliferation is signifi-cantly reduced in CFS patients as compared with controls. The b2-adrenergic receptor agonist terbutaline inhibits tumor necrosis fac-tor-a production and enhances interleukin-10 production by monocytes. Our data demonstrate that the capacity of a b2-adrenergic agonist to regulate the production of these two cytokines is also re-duced in CFS patients. We did not observe differences in baseline or