Are there alterations of neuroendocrine and cellular immune responses to nutrients in women with irritable bowel syndrome?
Date
2004
Authors
Elsenbruch, S.
Holtmann, G.
Oezcan, D.
Lysson, A.
Janssen, O.
Goebel, M.
Schedlowski, M.
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Journal article
Citation
American Journal of Gastroenterology, 2004; 99(4):703-710
Statement of Responsibility
Sigrid Elsenbruch, Gerald Holtmann, Deniz Oezcan, Andreas Lysson, Onno Janssen, Marion U Goebel and Manfred Schedlowski
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Abstract
OBJECTIVES: The goal was to investigate the neuroimmune axis in irritable bowel syndrome (IBS) by analyzing the neuroendocrine and cellular immune responses to nutrient load. METHODS: In the fasting state and 20, 40, 70, and 100 min following nutrient load, blood samples were collected and cardiovascular recordings were accomplished in 15 female IBS patients and 15 healthy women. Plasma norepinephrine, prolactin, cortisol, and growth hormone were analyzed, and blood pressure and heart rate responses were measured. The distribution of peripheral leukocytes and lymphocyte subpopulations and the in vitro production of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) after whole blood stimulation with in lipopolysaccharide (LPS) were analyzed. RESULTS: IBS patients demonstrated significantly greater postprandial increases in plasma norepinephrine and systolic blood pressure (p < 0.05), but no cortisol response. A postprandial redistribution of circulating leukocytes and lymphocyte subpopulations was observed in both groups, including significant increases in the numbers of leukocytes and granulocytes and significant decreases in the numbers of monocytes, T-cells, and natural killer (NK) cells (all p < 0.05). However, IBS patients demonstrated significantly greater postprandial increases in leukocytes and granulocytes, while changes in the numbers of monocytes and NK cells were significantly diminished (all p < 0.05). Patients also failed to show the postprandial decrease in the in vitro TNF-alpha production observed in controls. Postprandial norepinephrine concentrations were negatively correlated with NK cell numbers in IBS patients (r= 0.58, p < 0.05) but not controls. CONCLUSIONS: IBS may involve an autonomic hyper-responsiveness to visceral stimuli, which occurs throughout the entire gut, is independent of acutely perceived GI symptoms, and does not necessarily involve HPA axis activation. Women with IBS show altered cellular immune responses to food intake, which may at least in part be mediated by adrenergic mechanisms. Thus, autonomic disturbances may have implications for cellular immune function along the neuroendocrine-immune axis in patients with IBS.
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© 2004 The American College of Gastroenterology