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首页> 外文期刊>Infection and immunity >Shiga toxin-associated hemolytic-uremic syndrome: combined cytotoxic effects of Shiga toxin, interleukin-1 beta, and tumor necrosis factor alpha on human vascular endothelial cells in vitro.
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Shiga toxin-associated hemolytic-uremic syndrome: combined cytotoxic effects of Shiga toxin, interleukin-1 beta, and tumor necrosis factor alpha on human vascular endothelial cells in vitro.

机译：志贺毒素相关的溶血性尿毒症综合征：志贺毒素，白介素-1β和肿瘤坏死因子α在体外对人血管内皮细胞的综合细胞毒作用。

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This study explores the relationship between Shiga toxin-producing Shigella or Escherichia coli strains and the development of vascular complications in humans following bacillary dysentery. We propose that endotoxin-elicited interleukin-1 or tumor necrosis factor alpha (TNF) may combine with Shiga toxin to facilitate vascular damage characteristic of hemolytic-uremic syndrome. This study examines the cytotoxic effects of Shiga toxin, interleukin-1, and TNF on cultured human umbilical vein endothelial cells (HUVEC). Both Shiga toxin and TNF were cytotoxic to HUVEC, although HUVEC obtained from individual umbilical cords differed in their sensitivities to these agents. With Shiga toxin-sensitive HUVEC, combinations of TNF with Shiga toxin resulted in a synergistic cytotoxic effect. In contrast, interleukin-1 was not cytotoxic to HUVEC, nor did it enhance cell death in combination with Shiga toxin. The synergistic cytotoxic response of HUVEC to Shiga toxin and TNF was dose and time dependent for both agents and could be neutralized by monoclonal antibodies directed against either Shiga toxin or TNF. This synergistic response was delayed, being maximal on day 2. Preincubation (24 h) of HUVEC with TNF sensitized the cells to Shiga toxin. TNF alone had no effect on HUVEC protein synthesis but enhanced the inhibitory activity of Shiga toxin. These results are consistent with a role for Shiga toxin in the development of hemolytic-uremic syndrome at the level of the vascular endothelium in humans.
机译：这项研究探讨了产生志贺毒素的志贺氏菌或大肠杆菌菌株与细菌性痢疾后人血管并发症的发展之间的关系。我们建议内毒素引起的白介素1或肿瘤坏死因子α（TNF）可能与志贺毒素结合，以促进溶血尿毒综合征的血管损伤特征。这项研究检查了志贺毒素，白介素1和TNF对培养的人脐静脉内皮细胞（HUVEC）的细胞毒性作用。志贺毒素和TNF均对HUVEC具有细胞毒性，尽管从单个脐带获得的HUVEC对这些药物的敏感性有所不同。对于志贺毒素敏感的HUVEC，TNF与志贺毒素的组合可产生协同的细胞毒性作用。相比之下，白介素-1对HUVEC没有细胞毒性，与志贺毒素联合使用也不会增加细胞死亡。 HUVEC对志贺毒素和TNF的协同细胞毒性反应是剂量和时间依赖性的，并且可以被针对志贺毒素或TNF的单克隆抗体中和。该协同反应被延迟，在第2天达到最大。HUVEC与TNF的预温育（24 h）使细胞对志贺毒素敏感。单独的TNF对HUVEC蛋白合成没有影响，但增强了志贺毒素的抑制活性。这些结果与志贺毒素在人类血管内皮水平上在溶血性尿毒症综合征的发展中的作用一致。

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