McNamara B P, Donnenberg M S
Department of Medicine, University of Maryland School of Medicine, Baltimore 21201, USA.
FEMS Microbiol Lett. 1998 Sep 1;166(1):71-8. doi: 10.1111/j.1574-6968.1998.tb13185.x.
Enteropathogenic Escherichia coli (EPEC) cause a characteristic attaching and effacing (A/E) lesion in intestinal epithelial cells that is associated with the expression and export of specific bacterial proteins via a type III secretion pathway. These effector proteins and components of the type III export apparatus are encoded on a pathogenicity island known as the locus of enterocyte effacement (LEE). In this study, we describe a proline-rich protein, EspF, encoded by the LEE that is secreted by the EPEC type III secretion apparatus. Whereas an espF deletion mutant does not synthesize or secrete EspF, surprisingly it retains the ability to induce host signaling events, perform A/E activities, and invade host epithelial cells. Although these results do not indicate on obvious role for EspF in the formation of A/E lesions nor in the invasion of epithelial cells, they do not preclude a role played by EspF in other aspects of EPEC pathogenesis.
肠致病性大肠杆菌（EPEC）在肠道上皮细胞中引起一种特征性的黏附与抹消（A/E）损伤，这与特定细菌蛋白通过III型分泌途径的表达和输出有关。这些效应蛋白和III型输出装置的组分由一个称为肠上皮细胞抹消位点（LEE）的致病岛编码。在本研究中，我们描述了一种由LEE编码的富含脯氨酸的蛋白EspF，它由EPEC的III型分泌装置分泌。虽然espF缺失突变体不合成或分泌EspF，但令人惊讶的是，它仍保留诱导宿主信号事件、进行A/E活动以及侵入宿主上皮细胞的能力。尽管这些结果并未表明EspF在A/E损伤形成或上皮细胞侵袭中具有明显作用，但并不排除EspF在EPEC发病机制的其他方面发挥作用。
