Shiga toxin-producing Escherichia coli (STEC) causes outbreaks and sporadic cases of gastroenteritis. STEC O157:H7 is the most clinically relevant serotype in the world. The major virulence determinants of STEC O157:H7 are the Shiga toxins and the locus of enterocyte effacement. However, several accessory virulence factors, mainly outer membrane proteins (OMPs) that interact with the host cells may contribute to the virulence of this pathogen. Previously, the elongation factor thermo unstable (EF-Tu), l-asparaginase II and OmpT proteins were identified as antigens in OMP extracts of STEC. The known subcellular location of EF-Tu and l-asparaginase II are the cytoplasm and periplasm, respectively. Therefore, we investigate whether these two proteins may localize on the surface of STEC and, if so, what roles they have at this site. On the other hand, the OmpT protein, a well characterized protease, has been described as participating in the adhesion of extraintestinal pathogenic E. coli strains. Thus, we investigate whether OmpT has this role in STEC. Our results show that the EF-Tu and l-asparaginase II are secreted by O157:H7 and may also localize on the surface of this bacterium. EF-Tu was identified in outer membrane vesicles (OMVs), suggesting it as a possible export mechanism for this protein. Notably, we found that l-asparaginase II secreted by O157:H7 inhibits T-lymphocyte proliferation, but the role of EF-Tu at the surface of this bacterium remains to be elucidated. In the case of OmpT, we show its participation in the adhesion of O157:H7 to human epithelial cells. Thus, this study extends the knowledge of the pathogenic mechanisms of STEC.

中文翻译：

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解释产生志贺毒素的大肠杆菌的EF-Tu，1-天冬酰胺酶II和OmpT蛋白的其他作用。

产生志贺毒素的大肠埃希菌（STEC）引起暴发和肠胃炎的零星病例。STEC O157：H7是世界上临床上最相关的血清型。STEC O157：H7的主要毒力决定因素是志贺毒素和肠上皮细胞出现的部位。但是，一些辅助毒力因子，主要是与宿主细胞相互作用的外膜蛋白（OMP），可能会导致这种病原体的毒力。以前，将伸长因子热不稳定（EF-Tu），1-天冬酰胺酶II和OmpT蛋白鉴定为STEC OMP提取物中的抗原。EF-Tu和l的已知亚细胞位置-天冬酰胺酶II分别是细胞质和周质。因此，我们研究了这两种蛋白是否可能位于STEC的表面上，如果存在，那么它们在该位点起什么作用。另一方面，OmpT蛋白（一种特征明确的蛋白酶）已被描述为参与肠外致病性大肠杆菌菌株的粘附。因此，我们调查了OmpT在STEC中是否具有此作用。我们的结果表明，EF-Tu和1-天冬酰胺酶II由O157：H7分泌，并且也可能位于该细菌的表面。在外膜囊泡（OMVs）中鉴定出EF-Tu，表明它是该蛋白的可能出口机制。值得注意的是，我们发现，升O157：H7分泌的β-天冬酰胺酶II抑制T淋巴细胞的增殖，但该细菌表面的EF-Tu的作用尚待阐明。在OmpT的情况下，我们表明其参与O157：H7对人上皮细胞的粘附。因此，这项研究扩展了STEC的致病机理的知识。