A cloned pathogenicity island from enteropathogenic Escherichia coli confers the attaching and effacing phenotype on E. coli K‐12

McDaniel, Timothy K.; Kaper, James B.

doi:10.1046/j.1365-2958.1997.2311591.x

Cited by 501 publications

(421 citation statements)

References 28 publications

(62 reference statements)

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“…The ability to induce hypersensitive response in infected plants was transferred from plant-pathogenic Pseudomonas syringae pathovar syringae to P. fluorescens and E. coli by transfer of a cloned chromosomal locus (21). The LEE locus of enteropathogenic E. coli was transferred to an E. coli laboratory strain, and the LEE-dependent phenotypes were observed in cell culture models (27). Furthermore, pathogenicity islands encoding functions other than T3SS were transferred, e.g., the "high pathogenicity island" of a highly virulent strain of Yersinia enterocolitica to a low-virulence strain (36).…”

Section: Discussionmentioning

confidence: 99%

Functional Transfer of Salmonella Pathogenicity Island 2 to Salmonella bongori and Escherichia coli

2004

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The type III secretion system (T3SS) encoded by the Salmonella pathogenicity island 2 (SPI2) has a central role in systemic infections by Salmonella enterica and for the intracellular phenotype. Intracellular S. enterica uses the SPI2-encoded T3SS to translocate a set of effector proteins into the host cell, which modify host cell functions, enabling intracellular survival and replication of the bacteria. We sought to determine whether specific functions of the SPI2-encoded T3SS can be transferred to heterologous hosts Salmonella bongori and Escherichia coli Mutaflor, species that lack the SPI2 locus and loci encoding effector proteins. The SPI2 virulence locus was cloned and functionally expressed in S. bongori and E. coli. Here, we demonstrate that S. bongori harboring the SPI2 locus is capable of secretion of SPI2 substrate proteins under culture conditions, as well as of translocation of effector proteins under intracellular conditions. An SPI2-mediated cellular phenotype was induced by S. bongori harboring the SPI2 if the sifA locus was cotransferred. An interference with the host cell microtubule cytoskeleton, a novel SPI2-dependent phenotype, was observed in epithelial cells infected with S. bongori harboring SPI2 without additional effector genes. S. bongori harboring SPI2 showed increased intracellular persistence in a cell culture model, but SPI2 transfer was not sufficient to confer to S. bongori systemic pathogenicity in a murine model. Transfer of SPI2 to heterologous hosts offers a new tool for the study of SPI2 functions and the phenotypes of individual effectors.During the evolution of bacterial pathogenesis, the horizontal transfer of virulence genes has been a driving force for the emergence of new species and the adaptation of pathogens to new hosts and specific sites in these hosts. It has been concluded that large clusters of virulence genes are exchanged between various bacteria, and the acquisitions of so-called "pathogenicity islands" are considered as quantum leaps in the evolution of bacterial pathogenesis (13,35).Salmonella spp. form a complex group of gastrointestinal pathogens of animals and humans. Traditionally, a large number of isolates of Salmonella enterica have been defined as species due to distinct serological differences. However, molecular analyses indicated that most of these isolates represent serotypes of the species S. enterica, for example, S. enterica subspecies I serotype Typhimurium, and current taxonomy defines two species of Salmonella. Human infections are most frequently caused by various serovars of S. enterica. Disease outcomes associated with S. enterica can range from self-limiting localized gastrointestinal infections to life-threatening systemic infections such as typhoid fever (9). S. bongori, a second Salmonella species, is only rarely observed in human infections and is found as a commensal of cold-blooded animals (4, 38). Molecular analyses indicated that S. bongori represents a phylogenetically older separation from the genus Salmonella (4, 6).Beside...

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Section: Discussionmentioning

confidence: 99%

Functional Transfer of Salmonella Pathogenicity Island 2 to Salmonella bongori and Escherichia coli

2004

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“…EPEC possesses a unique 35 kbp pathogenicity island, the locus of enterocyte effacement (LEE), which contains all the genes needed to elicit the formation of AE lesions McDaniel and Kaper, 1997). Several classes of LEE genes have been described: the sep (secretion of EPEC proteins) genes, the esp (EPEC secreted proteins) genes and the eae gene .…”

Section: Introductionmentioning

confidence: 99%

Protein translocation into host epithelial cells by infecting enteropathogenic Escherichia coli

Wolff

Nisan

Hanski

et al. 1998

Molecular Microbiology

197

140

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SummaryEnteropathogenic Escherichia coli (EPEC) causes diarrhoea in young children. EPEC induces the formation of actin pedestal in infected epithelial cells. A type III protein secretion system and several proteins that are secreted by this system, including EspB, are involved in inducing the formation of the actin pedestals. We have demonstrated that contact of EPEC with HeLa cells is associated with the induction of production and secretion of EspB. Shortly after infection, EPEC initiates translocation of EspB, and EspB fused to the CyaA reporter protein (EspB-CyaA), into the host cell. The translocated EspB was distributed between the membrane and the cytoplasm of the host cell. Translocation was strongly promoted by attachment of EPEC to the host cell, and both attachment factors of EPEC, intimin and the bundle-forming pili, were needed for full translocation efficiency. Translocation and secretion of EspB and EspB-CyaA were abolished in mutants deficient in components of the type III protein secretion system, including sepA and sepB mutants. EspB-CyaA was secreted but not translocated by an espB mutant. These results indicate that EspB is both translocated and required for protein translocation by EPEC.

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“…Formation of AE lesions is involved with localized degeneration of the brush border microvilli and assembly of highly organized pedestallike actin structures in the epithelial cells beneath intimately attached bacteria . EPEC possesses a unique 35n6 kbp pathogenicity island, termed the locus of enterocyte effacement (LEE), that contains genes needed to elicit formation of AE lesions (McDaniel & Kaper, 1997). The LEE consists of 41 ORFs, organized in five major operons, LEE1 to LEE5, and several additional transcriptional units (Elliott et al, 1999(Elliott et al, , 1998McDaniel & Kaper, 1997).…”

Section: Introductionmentioning

confidence: 99%

“…EPEC possesses a unique 35n6 kbp pathogenicity island, termed the locus of enterocyte effacement (LEE), that contains genes needed to elicit formation of AE lesions (McDaniel & Kaper, 1997). The LEE consists of 41 ORFs, organized in five major operons, LEE1 to LEE5, and several additional transcriptional units (Elliott et al, 1999(Elliott et al, , 1998McDaniel & Kaper, 1997). These genes encode effector proteins and a type III secretion system, which functions as a molecular syringe to translocate effector proteins from the bacterial cytoplasm directly into the cytoplasm of host cells .…”

Section: Introductionmentioning

confidence: 99%

Thermoregulated expression of virulence genes in enteropathogenic Escherichia coli

2002

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Enteropathogenic Escherichia coli (EPEC) causes severe diarrhoea in young children. The locus of enterocyte effacement (LEE) pathogenicity island comprises a cluster of operons encoding a type III secretion system and related proteins that are associated with EPEC virulence. The LEE1 operon encodes Ler that positively regulates the LEE2, LEE3, LEE4, LEE5 and espG transcriptional units. The LEE operons are repressed at 27 SC and expressed at 37 SC. This paper describes a regulatory cascade of the thermoregulation of LEE operons. LEE1 including ler is repressed by H-NS at 27 SC but not at 37 SC. In contrast, the expression of the LEE2, LEE3, LEE4, LEE5 and espG transcriptional units is repressed by H-NS at both 27 SC and 37 SC. Upon shifting the culture temperature from 27 SC to 37 SC, Ler is synthesized and in turn activates the expression of LEE2, LEE3, LEE4 and espG by releasing the H-NS mediated repression. In the case of LEE5, Ler acts both by alleviating the H-NS mediated repression and by an additional mechanism, as yet to be defined.

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**A cloned pathogenicity island from enteropathogenic Escherichia coli confers the attaching and effacing phenotype on E. coli K‐12**

Cited by 501 publications

References 28 publications

Functional Transfer of Salmonella Pathogenicity Island 2 to Salmonella bongori and Escherichia coli

Functional Transfer of Salmonella Pathogenicity Island 2 to Salmonella bongori and Escherichia coli

Protein translocation into host epithelial cells by infecting enteropathogenic Escherichia coli

Thermoregulated expression of virulence genes in enteropathogenic Escherichia coli

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