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首页> 美国卫生研究院文献>Infection and Immunity >Up-Regulation of Both Intimin and eae-Independent Adherence of Shiga Toxigenic Escherichia coli O157 by ler and Phenotypic Impact of a Naturally Occurring ler Mutation
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Up-Regulation of Both Intimin and eae-Independent Adherence of Shiga Toxigenic Escherichia coli O157 by ler and Phenotypic Impact of a Naturally Occurring ler Mutation

机译：自然产生的ler突变的ler和表型影响对志贺毒素大肠杆菌O157的内膜素和独立于eae的粘附的上调

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Shiga toxigenic Escherichia coli (STEC) strains are important human pathogens which are capable of causing diarrhea, hemorrhagic colitis, and the potentially fatal hemolytic-uremic syndrome (HUS). An important virulence trait of certain STEC strains, such as those belonging to serogroup O157, is the capacity to produce attaching and effacing (A/E) lesions on enterocytes, a property encoded by the locus for enterocyte effacement (LEE). LEE contains the eae gene, which encodes intimin, an outer membrane protein which mediates the intimate attachment of bacteria to the host epithelial cell surface, and eae is routinely used as a marker for LEE-positive STEC strains. However, the O157:H− STEC strain 95SF2 carries eae but did not produce A/E lesions on HEp-2 cells, as judged by a fluorescent actin staining assay. In this assay, 95SF2 adhered poorly to the HEp-2 cells, and those that did bind exhibited abnormal cell division. In contrast, the O157:H7 STEC strain EDL933 adhered strongly and produced typical A/E lesions. We have demonstrated that 95SF2 carries a defective LEE regulatory gene, ler, with a single base change with respect to that published for ler of EDL933, resulting in an Ile57-to-Thr substitution. Ler shows homology to H-NS-like regulators, which are modulators of transcription, and the mutation occurs in a domain implicated in oligomerization. 95SF2 was able to adhere and produce A/E lesions on HEp-2 cells when EDL933 ler was expressed from a multicopy plasmid. Conversely, introduction of a plasmid carrying 95SF2 ler into EDL933 abolished adherence and capacity to form A/E lesions. Studies with eae deletion derivatives of 95SF2 and EDL933 demonstrated that the ler-mediated adherence to HEp-2 cells is largely independent of intimin. We have also demonstrated that EDL933 ler, but not 95SF2 ler, increases the level of intimin in O157 STEC.
机译：志贺毒素性大肠杆菌（STEC）菌株是重要的人类病原体，能够引起腹泻，出血性结肠炎和潜在致命的溶血性​​尿毒症综合征（HUS）。某些STEC菌株（如O157血清型的菌株）的重要毒力特征是在肠上皮细胞上产生附着和脱落（A / E）损伤的能力，这是由肠上皮细胞脱落（LEE）的基因座编码的特性。 LEE包含eae基因，该基因编码intimin，一种外膜蛋白，介导细菌与宿主上皮细胞表面的紧密附着，eae通常用作LEE阳性STEC菌株的标记。但是，O157：H - STEC菌株95SF2携带eae，但在HEp-2细胞上未产生A / E病变，这是通过荧光肌动蛋白染色分析判断的。在该测定中，95SF2与HEp-2细胞的粘附性很差，而那些结合的细胞表现出异常的细胞分裂。相反，O157：H7 STEC菌株EDL933牢固粘附并产生典型的A / E病变。我们已经证明95SF2携带有缺陷的LEE调节基因ler，相对于EDL933的ler而言，具有单一碱基变化，从而导致Ile57到Thr取代。 Ler与作为转录调节剂的H-NS-like调节子具有同源性，并且该突变发生在涉及寡聚化的结构域中。当从多拷贝质粒表达EDL933ler时，95SF2能够在HEp-2细胞上粘附并产生A / E损伤。相反，将携带95SF2ler的质粒导入EDL933消除了粘附和形成A / E病变的能力。用95SF2和EDL933的eae缺失衍生物进行的研究表明，ler介导的对HEp-2细胞的粘附在很大程度上独立于内膜素。我们还证明了EDL933而不是95SF2会增加O157 STEC中内膜素的水平。

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