摘要目的毒源性大肠杆菌(VTEC)O157∶H7株的感染可以引起许多疾病的发生,这些疾病包括有出血性痢疾和溶血性尿毒症(HUS)等.为进一步揭示该菌株产生的V毒素在溶血性尿毒症和其他VTEC相关疾病中的病理性损伤作用,我们研究了基因重组的V2毒素(rVT2)对中性粒细胞生物学活性的影响.方法在这项研究中,我们运用了流式细胞技术、荧光标记探针--BCECF/AM和细胞色素c还原法测定超氧离子(O2-)技术.结果重组V2毒素对中性粒细胞自发性凋亡有显著的抑制作用,与此同时,这些中性粒细胞仍然保留多种生物学活性,如:细胞表面粘附分子的表达(CD62L减少、CD11b/CD18增加),粘附人脐带静脉血管内皮细胞(HUVEC)以及产生超氧离子(O2-).结论 V2毒素可延长中性粒细胞的功能性生命期限,加重局部炎症反应,这可能是溶血性尿毒症和VTEC相关疾病发生过程中中性粒细胞介导组织损伤的一个重要因素.

abstractsObjective Verotoxin-producing Escherichia coli (VTEC) strains of serotype O157∶H7 have been implicated in a wide spectrum of diseases, including blood diarrhea, hemorrhagic colitis and hemolytic uremic syndrome (HUS). To further explore the pathological role of verotoxin (VT) in HUS and other VTEC-associated diseases, we investigated the effects of recombinant verotoxin 2 (rVT2) on the biological activity of neutrophils.Methods The technique of flow cytometry, a fluorescent probe 2,7-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein acetoxymethyl ester (BCECF/AM), and the assay of reduced cytochrome c to detect superoxide production were used in this study. Results rVT2 significantly inhibited spontaneous apoptosis in neutrophils. Neutrophils with prolonged survival due to rVT2 maintained various biological functions, such as the expression of adhesion molecules (shading CD62L and raising CD11b/CD18), adherence to human umbilical vein endothelial cells (HUVECs), and generation of superoxide (O2 ). Conclusion Prolongation of the functional life-span of neutrophils by rVT2 may accelerate inflammatory responses at sites of inflammation. This may play a crucial role in neutrophil-mediated tissue injury in HUS and other VTEC-associated diseases.