Women with IBS show altered cellular immune responses to food intake

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Am J Gastroenterol. 2004 Apr;99(4):703-10.

Are there alterations of neuroendocrine and cellular immune responses to

nutrients in women with irritable bowel syndrome?

Elsenbruch S, Holtmann G, Oezcan D, Lysson A, Janssen O, Goebel MU,

Schedlowski M.

Department of Medical Psychology, University Clinic of Essen, Essen,

Germany.

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.

PMID: 15089905 [PubMed - indexed for MEDLINE]

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