Elsenbruch Sigrid, Holtmann Gerald, Oezcan Deniz, Lysson Andreas, Janssen Onno, Goebel Marion U, Schedlowski Manfred
Department of Medical Psychology, University Clinic of Essen, Essen, Germany.
Am J Gastroenterol. 2004 Apr;99(4):703-10. doi: 10.1111/j.1572-0241.2004.04138.x.
The goal was to investigate the neuroimmune axis in irritable bowel syndrome (IBS) by analyzing the neuroendocrine and cellular immune responses to nutrient load.
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.
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.
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.
通过分析对营养负荷的神经内分泌和细胞免疫反应，研究肠易激综合征（IBS）中的神经免疫轴。
在空腹状态以及营养负荷后20、40、70和100分钟，采集15名女性IBS患者和15名健康女性的血样并进行心血管记录。分析血浆去甲肾上腺素、催乳素、皮质醇和生长激素，并测量血压和心率反应。分析外周白细胞和淋巴细胞亚群的分布以及用脂多糖（LPS）全血刺激后体外肿瘤坏死因子α（TNF-α）和白细胞介素6（IL-6）的产生。
IBS患者餐后血浆去甲肾上腺素和收缩压显著升高（p<0.05），但无皮质醇反应。两组均观察到循环白细胞和淋巴细胞亚群的餐后重新分布，包括白细胞和粒细胞数量显著增加，单核细胞、T细胞和自然杀伤（NK）细胞数量显著减少（均p<0.05）。然而，IBS患者餐后白细胞和粒细胞增加显著更多，而单核细胞和NK细胞数量的变化显著减小（均p<0.05）。患者也未表现出对照组中观察到餐后体外TNF-α产生的减少。IBS患者餐后去甲肾上腺素浓度与NK细胞数量呈负相关（r=0.58，p<0.05），而对照组无此相关性。
IBS可能涉及对内脏刺激的自主神经高反应性，这种反应发生在整个肠道，独立于急性感知的胃肠道症状，且不一定涉及下丘脑-垂体-肾上腺（HPA）轴激活。IBS女性对食物摄入的细胞免疫反应发生改变，这可能至少部分由肾上腺素能机制介导。因此，自主神经紊乱可能对IBS患者神经内分泌-免疫轴上的细胞免疫功能产生影响。
