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首页> 外文期刊>Clinical kidney journal. >Cholinergic anti-inflammatory pathway activity in dialysis patients: a role for neuroimmunomodulation?
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Cholinergic anti-inflammatory pathway activity in dialysis patients: a role for neuroimmunomodulation?

机译：透析患者的胆碱能抗炎途径活性：神经免疫调节作用？

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Background The cholinergic anti-inflammatory pathway (CAP) modulates inflammatory responses through the vagus nerve and the α-7-nicotinic acetylcholine receptor (α7nAChR) on macrophages and immune cells. Sympathetic/parasympathetic imbalance and chronic inflammation are both linked to poor outcome in dialysis patients. The aim of this study was to investigate CAP activity in these patients. Methods Twenty dialysis patients, 12 hemodialysis (HD) and 8 peritoneal dialysis (PD) patients (12 male, 8 female; age range 47–83 years) and 8 controls (5 male, 3 female; age range 31–52 years) were analyzed for C-reactive protein (CRP), tumor necrosis factor (TNF), interleukin-1b (IL-1b), IL-6 and IL-10 at baseline. The cytokines were then assessed after whole blood stimulation ex vivo with lipopolysaccharide (LPS) (10 and 100 ng/mL) and again in the presence of 45 and 90 μmol/L GTS-21, a cholinergic α7nAChR agonist. Results CRP, TNF, IL-1 and IL-6 were significantly higher, whereas IL-10 was significantly lower at baseline in patients compared with controls. After LPS stimulation, TNF increased significantly more in patients than in controls but decreased to similar levels in both groups after addition of GTS-21. IL-6 attenuation was comparable with TNF and the IL-1b pattern was similar but remained significantly higher in patients. Interestingly, IL-10 increased after GTS-21 in a dose-dependent manner, but only in patients. Results in HD and PD patients did not differ. Conclusions The response of immune cells after LPS exposure and cholinergic stimulation suggests a functional CAP in dialysis patients. It may thus be possible to target the α7nAChR control of cytokine release as an anti-inflammatory strategy and thereby improve outcome in these patients.
机译：背景胆碱能抗炎途径（CAP）通过巨噬细胞和免疫细胞上的迷走神经和α-7烟碱乙酰胆碱受体（α7nAChR）调节炎症反应。交感/副交感神经失调和慢性炎症均与透析患者的不良预后有关。这项研究的目的是调查这些患者的CAP活性。方法20例透析患者，12例血液透析（HD）和8例腹膜透析（PD）患者（男12例，女8例;年龄47-83岁）和8例对照（男5例，女3例;年龄31-52岁）在基线时分析了C反应蛋白（CRP），肿瘤坏死因子（TNF），白介素-1b（IL-1b），IL-6和IL-10。在用脂多糖（LPS）（10和100 ng / mL）进行全血体外刺激后，再在存在胆碱能α7nAChR激动剂45和90μmol/ L GTS-21的情况下，再次评估细胞因子。结果与对照组相比，基线时患者的CRP，TNF，IL-1和IL-6显着升高，而IL-10显着降低。 LPS刺激后，患者中TNF的增加明显高于对照组，但在添加GTS-21后两组中的TNF下降至相似水平。 IL-6衰减与TNF相当，IL-1b模式相似但在患者中仍显着较高。有趣的是，GTS-21后IL-10以剂量依赖性方式增加，但仅在患者中增加。 HD和PD患者的结果无差异。结论LPS暴露和胆碱能刺激后免疫细胞的应答提示透析患者可使用CAP。因此，有可能将α7nAChR控制细胞因子的释放作为抗炎策略，从而改善这些患者的预后。

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