title: Stress-related peripheral neuroendocrine-immune interactions in women with ulcerative colitis.
abstract: OBJECTIVE
  The mechanisms underlying the interaction of psychological stress with the disease course in inflammatory bowel diseases remain unclear. We analyzed the neuroendocrine and cellular immune responses to public speaking stress, and the in vitro adrenergic and glucocorticoid modulation of cytokine production by peripheral blood cells (PBCs) in women with ulcerative colitis (UC) compared to healthy female controls.
  
  
  METHODS
  In 22 female UC patients with inactive disease or mild disease activity and 24 healthy females we analyzed the neuroendocrine and cellular immune responses to public speaking stress and the vitro beta-adrenergic and glucocorticoid regulation of IL-10 and TNF-alpha production by PBCs.
  
  
  RESULTS
  Public speaking stress-induced neuroendocrine and sympatho-adrenal activation, as well as the redistribution of circulating leukocytes were comparable in UC and controls. Significant but comparable public speaking stress-induced increases in LPS-stimulated TNF-alpha and IL-10, as well as in CD2/CD28-stimulated IFN-gamma were observed in both groups. UC demonstrated significantly reduced baseline IFN-gamma production, as well as significantly lower basal cortisol and prolactin levels. The in vitro beta-adrenergic stimulation of PBCs revealed reduced IL-10 response in UC.
  
  
  CONCLUSIONS
  Psychosocial stress-induced activation of the neuroendocrine and sympatho-adrenal systems remain unaltered in UC, suggesting that the mechanism(s) mediating effects of psychological stress on disease activity are likely operative downstream at the level of the intestine. However, UC patients show disturbances in basal endocrine and cytokine measures. Together with our in vitro evidence of disturbed adrenergic regulation of IL-10 production by stimulated PBCs in UC, these may indicate the existence of subtle disturbance of peripheral cellular neuroendocrine-immune interactions in UC.
authors.affiliation: Department of Internal & Integrative Medicine, Kliniken Essen Mitte, University of Duisburg-Essen, Germany.
authors.forename: Jost
authors.initials: J
authors.lastname: Langhorst
authors.forename: Pieter M
authors.initials: PM
authors.lastname: Cobelens
authors.forename: Annemieke
authors.initials: A
authors.lastname: Kavelaars
authors.forename: Cobi J
authors.initials: CJ
authors.lastname: Heijnen
authors.forename: Sven
authors.initials: S
authors.lastname: Benson
authors.forename: Nadja
authors.initials: N
authors.lastname: Rifaie
authors.forename: Gustav J
authors.initials: GJ
authors.lastname: Dobos
authors.forename: Manfred
authors.initials: M
authors.lastname: Schedlowski
authors.forename: Sigrid
authors.initials: S
authors.lastname: Elsenbruch
mesh_terms: D000293:Adolescent; D000328:Adult; D002478:Cells, Cultured; D003093:Colitis, Ulcerative / Q000150:complications* / Q000276:immunology / Q000503:physiopathology*; D003907:Dexamethasone / Q000494:pharmacology; D004912:Erythrocytes / Q000187:drug effects; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D007107:Immune System / Q000502:physiology*; D018655:Lymphocyte Count; D008214:Lymphocytes / Q000187:drug effects; D008875:Middle Aged; D009483:Neuropsychological Tests; D009490:Neurosecretory Systems / Q000502:physiology*; D013060:Speech; D013315:Stress, Psychological / Q000150:complications* / Q000276:immunology / Q000503:physiopathology*; D013566:Sympathomimetics / Q000494:pharmacology; D013726:Terbutaline / Q000494:pharmacology
chemical_list: D005938:Glucocorticoids; D013566:Sympathomimetics; D003907:Dexamethasone; D013726:Terbutaline