Trabold B, Rothoerl R, Wittmann S, Woertgen C, Fröhlich D
Klinik für Anästhesiologie, Universität Regensburg, Regensburg, Deutschland.
Neuroimmunomodulation. 2005;12(3):152-6. doi: 10.1159/000084847.
To investigate the effect of cerebrospinal fluid (CSF) from patients with subarachnoid hemorrhage (SAH) on the activation of polymorphonuclear neutrophils (PMN) in response to receptor-dependent stimulation with N-formyl-l-methionyl-l-leucyl-l-phenylalanine and TNFalpha or non-receptor-dependent stimulation with phorbol 12-myristate 13-acetate.
CSF from 12 patients with SAH due to ruptured cerebral aneurysm was collected. Samples of CSF were drawn at different time points. CSF from 6 healthy subjects receiving spinal anesthesia served as the control group. After stimulation of PMN the generation of reactive oxygen intermediates was analyzed on a flow cytometer.
In the presence of CSF, PMN showed a significant suppression of the oxidative burst following stimulation compared to stimulation without CSF. The reduction of the oxidative burst following stimulation was higher in the presence of CSF from patients with SAH. After pretreatment at 56 degrees C, the extent of the suppression observed following receptor-dependent stimulation and CSF from patients with SAH was similar to that seen after stimulation with CSF from healthy individuals.
These data show that the presence of CSF resulted in a suppression of neutrophil oxidative function. A more distinct depression was seen in the presence of CSF from patients with SAH. We suggest a complex physiological inhibitory and protective mechanism against unfavorable activation of PMN by CSF.
研究蛛网膜下腔出血(SAH)患者的脑脊液(CSF)对多形核中性粒细胞(PMN)在受到N-甲酰-L-蛋氨酰-L-亮氨酰-L-苯丙氨酸和肿瘤坏死因子α(TNFα)受体依赖性刺激或佛波酯12-肉豆蔻酸酯13-乙酸酯非受体依赖性刺激时激活的影响。
收集12例因脑动脉瘤破裂导致SAH患者的脑脊液。在不同时间点采集脑脊液样本。6例接受脊髓麻醉的健康受试者的脑脊液作为对照组。刺激PMN后,在流式细胞仪上分析活性氧中间体的生成。
与无脑脊液刺激相比,在有脑脊液存在的情况下,PMN在刺激后显示出氧化爆发的显著抑制。在SAH患者的脑脊液存在下,刺激后氧化爆发的降低更高。在56℃预处理后,受体依赖性刺激和SAH患者脑脊液刺激后观察到的抑制程度与健康个体脑脊液刺激后相似。
这些数据表明脑脊液的存在导致中性粒细胞氧化功能受到抑制。在SAH患者的脑脊液存在下观察到更明显的抑制。我们提出脑脊液对PMN不良激活具有复杂的生理抑制和保护机制。