Annemieke Kavelaars, Wietse Kuis, Lidewij Knook, Gerben Sinnema and Cobi J. Heijnen
Departments of Pediatric Immunology (A.K., W.K., L.K., C.J.H.) and Psychology (G.S.), Wilhelmina Children’s Hospital of the University Medical Center Utrecht, 3584 EA Utrecht, The Netherlands
Address correspondence and requests for reprints to: Dr. Annemieke Kavelaars, Wilhelmina Children’s Hospital of the University Medical Center Utrecht, Department of Pediatric Immunology, Room KC 03.068.0, Lundlaan 6, 3584 EA Utrecht, The Netherlands. E-mail: email@example.com.
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 ß2-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 significantly reduced in CFS patients as compared with controls.
The ß2-adrenergic receptor agonist terbutaline inhibits tumor necrosis factor- production and enhances interleukin-10 production by monocytes. Our data demonstrate that the capacity of a ß2-adrenergic agonist to regulate the production of these two cytokines is also reduced in CFS patients. We did not observe differences in baseline or CRH-induced cortisol and ACTH between CFS patients and controls. Baseline noradrenaline was similar in CFS and controls, whereas baseline adrenaline levels were significantly higher in CFS patients.
We conclude that CFS is accompanied by a relative resistance of the immune system to regulation by the neuroendocrine system. Based on these data, we suggest CFS should be viewed as a disease of deficient neuroendocrine-immune communication.