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重组V2毒素延长中性粒细胞的功能性生命期限
引用本文:刘佳佳,曾付兰,谢华福,段承刚,甘琳,李娟,宋杰,赤星透,近滕启文.重组V2毒素延长中性粒细胞的功能性生命期限[J].泸州医学院学报,2001,24(5):365-369.
作者姓名:刘佳佳  曾付兰  谢华福  段承刚  甘琳  李娟  宋杰  赤星透  近滕启文
作者单位:1. 泸州医学院中心实验室,
2. 泸州医学院附属医院检验科,
3. 日本北里大学医学部内科
基金项目:日本文部省科研基金资助 (10 6 70 42 3)
摘    要:目的:揭示V毒素在溶血性尿毒症(HUS)和其他与多源性大肠杆菌(VTEC)相关疾病中的病理性损伤作用。方法:运用流式细胞技术,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(rVT2)对中性粒细胞自发性凋亡有着显著性的抑制作用。被rVT2延迟了凋亡的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减少和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毒素延长中性粒细胞的功能性生命期限,会加重炎症局部的炎症反应,这可能是HUS和VTEC相关疾病的发生过程中,中性粒细胞介导的组织损伤的一个重要因素。

关 键 词:中性粒细胞  V2毒素  溶血性尿毒症  VTEC相关疾病  功能
文章编号:1000-2669(2001)05-0365-05

PROLONGATION OF THE FUNCTIONAL LIFE-SPAN OF NEUTROPHILS BY RECOMBINANT VEROTOXIN 2
Liu Jiajia,et al Central Laboratory of Luzhou Medical College.PROLONGATION OF THE FUNCTIONAL LIFE-SPAN OF NEUTROPHILS BY RECOMBINANT VEROTOXIN 2[J].Journal of Luzhou Medical College,2001,24(5):365-369.
Authors:Liu Jiajia  Central Laboratory of Luzhou Medical College
Abstract:Objective: Verotoxin-producing Escherichia coli (VTEC) strains of serotype O157:H7 have been implicated as causes of a wide spectrum of diseases, raging from blood diarrhea and hemorrhagic colitis to hemolytic uremic syndrome (HUS). Recent studies have demonstrated that a direct cytotoxic effect of verotoxins (VTs) is related in the diseases. We previously reported the inhibitory effect of VT 2 on spontaneous apoptosis of neutrophils. To further reveal the pathological role of verotoxin (VT) in HUS and other VTEC-associated diseases, the effects of recombinant VT 2 (rVT 2) on the biological activities of neutrophils are investigated. Methods: The technique of FACS flow cytometer, a fluorescent probe-BCECF/ AM, and the assay of reduced cytochrome c to detect superoxide production were used in this study. Results: rVT 2 significantly inhibited spontaneous apoptosis of neutrophils. Neutrophils whose apoptosis had been delayed rVT 2 maintained various biological functions, such as expression of adhesion molecules (shading CD62L and raising CD11b/CD18), adherence to human umbilical vein endothelial cells (HUVEC), and generation of superoxide (O-2). Conclusion: Prolongation of the functional life-span of neutrophils by rVT 2 may accelerate inflammatory responses in sites of inflammation, which may play a crucial role in neutrophil-mediated tissue injury in HUS and other VTEC-associated diseases.
Keywords:Neutrophils  Verotoxin 2  Hemolytic uremic syndrome (HUS)  VTEC-associated diseases  Functions of neutrophils
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