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Int J Med Microbiol. 2004 Sep;294(2-3):103-13.

Impact of the locus of enterocyte effacement pathogenicity island on the evolution of pathogenic Escherichia coli.

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  • 1Institut für Mikrobiologie und Tierseuchen, Freie Universität Berlin, D-10061 Berlin, Germany. jores@web.de


This review summarizes our current knowledge and models of appearance and dissemination of the locus of enterocyte effacement (LEE) within Escherichia coli phylogenetic lineages. The LEE is a pathogenicity island (PAI) required for attaching and effacing (A/E) lesion formation induced on epithelial cells of humans and animals by enteropathogenic and numerous enterohemorrhagic E. coli strains as well as other related bacteria. The LEE encodes a type III secretion system, an adhesin (intimin) responsible for the intimate attachment of the bacteria to the cell and a number of secreted proteins involved in signal transduction events. It has been shown that the LEE varies in size from 36 to 111 kb, depending on what E. coli lineages carrying that PAI. Three tRNA genes are known as LEE integration sites selC, pheU and pheV, the latter two are identical in sequence. Beneath its functional role, intimin is considered a phylogenetic marker of the LEE. Currently, 14 different intimin types have been described, designated alpha through ksi. Beta intimin-carrying LEEs moved within certain E. coli lineages from the pheU tRNA gene into the pheV tRNA gene. Moreover, as a result of the typing of multiple LEE core regions, the appearance of two different LEE cores indicates an import of the LEE within E. coli at least two times.

[PubMed - indexed for MEDLINE]
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