Influence of first and long-term dialysis on uraemia-associated increased basal production of interleukin-1 and tumour necrosis factor alpha by circulating monocytes.

Influence of first and long-term dialysis on uraemia-associated increased basal production of interleukin-1 and tumour necrosis factor alpha by circulating monocytes.
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首次和长期透析对尿毒症相关的循环单核细胞白介素-1 和肿瘤坏死因子 α 基础产量增加的影响。

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发表时间:
1991
影响因子:
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通讯作者:
B. Descamps
B. Descamps
中科院分区:
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文献类型:
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作者:
A. Herbelin;P. Ureña;A. Nguyen;J. Zingraff;B. Descamps

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在之前的一项研究中,我们证实了长期血液透析患者中循环白细胞介素-1 (IL-1)的存在,以及长期血液透析和未透析尿毒症患者中循环肿瘤坏死因子α (TNF - α)的存在。本报告研究了35例长期血液透析患者和36例首次透析的尿毒症患者的单核细胞自发产生和分泌这两种细胞因子的能力。与正常人相比,长期血液透析和首次透析尿毒症患者透析前新分离单核细胞中与细胞相关的IL-1浓度均显著升高。在两组中,与正常个体相比,尽管在新鲜分离的单核细胞中无法检测到细胞内TNF - α,但在无外源刺激和无血清条件下,单核细胞体外培养20小时后,细胞外IL-1和TNF - α浓度均大大增加。然而,长期血液透析患者的IL-1分泌值高于未透析的尿毒症患者。在长期血液透析患者中,在单次透析期间,细胞相关和分泌的IL-1均显著增加,但TNF - α未显著增加。相比之下,在尿毒症患者第一次透析结束时,两种细胞因子的浓度都没有变化。我们的研究结果强烈提示与尿毒症相关的因素可能是启动细胞内IL-1蛋白合成和单核细胞释放TNF - α的充分信号,但在周期性血液透析过程中可能会刺激更多的IL-1释放。
In a previous study we demonstrated the presence of circulating interleukin-1 (IL-1) in long-term haemodialysis patients and of tumour necrosis factor alpha (TNF alpha) in both long-term haemodialysis and not-yet-dialysed uraemic patients. The present report investigates the spontaneous capacity of monocytes to produce and secrete these two cytokines in 35 long-term haemodialysis patients and 36 uraemic patients undergoing their first dialysis session. Predialytic cell-associated IL-1 concentrations in freshly isolated monocytes were significantly increased both in long-term haemodialysis and first-dialysis uraemic patients compared to normal individuals. In both groups in comparison to normal individuals, although intracellular TNF alpha could not be detected in freshly isolated monocytes, both extracellular IL-1 and TNF alpha concentrations were greatly increased after 20 h of in vitro culture of monocytes in the absence of exogenous stimulation and in serum-free conditions. However, long-term haemodialysis patients showed higher values of secreted IL-1 than not-yet dialysed uraemic patients. During a single dialysis session a significant increase in both cell-associated and secreted IL-1 but not TNF alpha was observed in long-term haemodialysis patients. In contrast, no change in the concentration of either cytokine could be detected at the end of the first dialysis session in uraemic patients. Our findings strongly suggest that factors related to uraemia could be a sufficient signal to initiate intracellular IL-1 protein synthesis and TNF alpha release by monocytes, but that greater IL-1 release could be stimulated during the periodic haemodialysis procedure.