Shiga toxins present in the gut and in the polymorphonuclear leukocytes circulating in the blood of children with hemolytic-uremic syndrome

Shiga toxins present in the gut and in the polymorphonuclear leukocytes circulating in the blood of children with hemolytic-uremic syndrome
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DOI:
10.1128/jcm.44.2.313-317.2006
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发表时间:
2006-02-01
影响因子:
9.4
通讯作者:
Rizzoni, G
Rizzoni, G
中科院分区:
医学2区
文献类型:
--
作者:
Brigotti, M;Caprioli, A;Rizzoni, G

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溶血性尿毒症综合征是儿童早期急性肾衰竭的主要原因,主要是由某些产生滋贺毒素的大肠杆菌菌株引起的肠道感染引起的。在肠道中释放的毒素在与多形核白细胞结合后靶向肾内皮。采用Vero细胞毒试验和流式细胞术检测了20例溶血尿毒综合征患儿粪便和外周血中性粒细胞中滋贺毒素的含量。后者显示13名患者的多形核白细胞上存在滋贺毒素,其中5名患者没有其他微生物学或血清学证据表明产滋贺毒素大肠杆菌感染。在肠腔中释放的滋贺毒素量与在血流中释放的量之间观察到正相关。在粪便中检测不到毒素后,中性粒细胞上可检测到毒素的中位时间为5天。本研究证实中性粒细胞上滋贺毒素的免疫检测是溶血性尿毒症综合征中产滋贺毒素大肠杆菌感染的实验室诊断的有价值的工具,并为进一步研究中性粒细胞在该综合征发病机制中的作用提供线索。
Hemolytic-uremic syndrome, the main cause of acute renal failure in early childhood, is caused primarily by intestinal infections from some Escherichia coli strains that produce Shiga toxins. The toxins released in the gut are targeted to renal endothelium after binding to polymorphonuclear leukocytes. The presence of Shiga toxins in the feces and the circulating neutrophils of 20 children with hemolytic uremic syndrome was evaluated by the Vero cell cytotoxicity assay and flow cytometric analysis, respectively. The latter showed the presence of Shiga toxins on the polymorphonuclear leukocytes of 13 patients, 5 of whom had no other microbiologic or serologic evidence of infection by Shiga toxin-producing Escherichia coli. A positive relationship was observed between the amounts of Shiga toxins released in the intestinal lumen and those released in the bloodstream. The toxins were detectable on the neutrophils for a median period of 5 days after they were no longer detectable in stools. This investigation confirms that the immunodetection of Shiga toxins on neutrophils is a valuable tool for laboratory diagnosis of Shiga toxin-producing Escherichia coli infection in hemolytic-uremic syndrome and provides clues for further studies on the role of neutrophils in the pathogenesis of this syndrome.