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首页> 美国卫生研究院文献>Infection and Immunity >Shiga Toxin 2 Reduces Complement Inhibitor CD59 Expression on Human Renal Tubular Epithelial and Glomerular Endothelial Cells
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Shiga Toxin 2 Reduces Complement Inhibitor CD59 Expression on Human Renal Tubular Epithelial and Glomerular Endothelial Cells

机译：志贺毒素2减少人类肾小管上皮和肾小球内皮细胞的补体抑制剂CD59表达。

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摘要

Infections with enterohemorrhagic Escherichia coli (EHEC) are a primary cause of hemolytic-uremic syndrome (HUS). Recently, Shiga toxin 2 (Stx2), the major virulence factor of EHEC, was reported to interact with complement, implying that the latter is involved in the pathogenesis of EHEC-induced HUS. The aim of the present study was to investigate the effect of Stx2 on the expression of membrane-bound complement regulators CD46, CD55, and CD59 on proximal tubular epithelial (HK-2) and glomerular endothelial (GEnC) cells derived from human kidney cells that are involved in HUS. Incubation with Stx2 did not influence the amount of CD46 or CD55 on the surface of HK-2 and GEnC cells, as determined by fluorescence-activated cell sorter analysis. In contrast, CD59 was significantly reduced by half on GEnC cells, but the reduction on HK-2 cells was less pronounced. With increasing amounts of Stx2, reduction of CD59 also reached significance in HK-2 cells. Enzyme-linked immunosorbent assay analyses showed that CD59 was not present in the supernatant of Stx2-treated cells, implying that CD59 reduction was not caused by cleavage from the cell surface. In fact, reverse transcription-quantitative PCR analyses showed downregulation of CD59 mRNA as the likely reason for CD59 cell surface reduction. In addition, a significant increase in terminal complement complex deposition on HK-2 cells was observed after treatment with Stx2, as a possible consequence of CD59 downregulation. In summary, Stx2 downregulates CD59 mRNA and protein levels on tubular epithelial and glomerular endothelial cells, and this downregulation likely contributes to complement activation and kidney destruction in EHEC-associated HUS.
机译：肠出血性大肠杆菌（EHEC）感染是溶血性尿毒症综合征（HUS）的主要原因。最近，据报道，EHEC的主要毒力因子志贺毒素2（Stx2）与补体相互作用，这暗示后者参与EHEC诱导的HUS的发病机理。本研究的目的是研究Stx2对人肾细胞来源的近端肾小管上皮细胞（HK-2）和肾小球内皮细胞（GEnC）细胞膜结合的补体调节因子CD46，CD55和CD59表达的影响。参与HUS。通过荧光激活细胞分选仪分析确定，与Stx2一起孵育不会影响HK-2和GEnC细胞表面CD46或CD55的量。相反，CD59在GEnC细胞上显着减少了一半，但在HK-2细胞上的减少却不那么明显。随着Stx2量的增加，CD59的减少在HK-2细胞中也达到了显着水平。酶联免疫吸附试验分析表明，经Stx2处理的细胞上清液中不存在CD59，这表明CD59的减少不是由于从细胞表面分裂而引起的。实际上，逆转录定量PCR分析显示CD59 mRNA的下调是CD59细胞表面减少的可能原因。另外，在用Stx2处理后，观察到HK-2细胞上末端补体复合物沉积的显着增加，这是CD59下调的可能结果。总之，Stx2下调肾小管上皮和肾小球内皮细胞上CD59 mRNA和蛋白的水平，这种下调可能有助于补充EHEC相关HUS的激活和肾脏破坏。

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