Stress-related peripheral neuroendocrine-immune interactions in women with ulcerative colitis

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doi:10.1016/j.psyneuen.2007.09.003 Copyright © 2007 Elsevier Ltd All rights reserved.

Stress-related peripheral neuroendocrine–immune interactions in women with ulcerative colitis

Jost Langhorsta, Pieter M. Cobelensb, Annemieke Kavelaarsb, Cobi J. Heijnenb, Sven Bensonc, Nadja Rifaiec, Gustav J. Dobosa, Manfred Schedlowskic and Sigrid Elsenbruchc, , aDepartment of Internal & Integrative Medicine, Kliniken Essen Mitte, University of Duisburg-Essen, GermanybDepartment of Psychoneuroimmunology, University Medical Center Utrecht, The NetherlandscDepartment of Medical Psychology & Behavioral Immunobiology, University Hospital of Essen, University of Duisburg-Essen, Hufelandstr. 55, 45122 Essen, Germany Received 11 June 2007; revised 5 September 2007; accepted 6 September 2007. Available online 22 October 2007.

Summary

Objectives

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 β-adrenergic and glucocorticoid regulation of IL-10 and TNF-α 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-α and IL-10, as well as in CD2/CD28-stimulated IFN-γ were observed in both groups. UC demonstrated significantly reduced baseline IFN-γ production, as well as significantly lower basal cortisol and prolactin levels. The in vitro β-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.

Keywords: Inflammatory bowel diseases; Ulcerative colitis; Psychological stress; Hypothalamic–pituitary–adrenal-axis; Glucocorticoid sensitivity; Cytokines

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Psychoneuroendocrinology Volume 32, Issues 8-10, September-November 2007, Pages 1086-1096