Journal Article10.1046/J.1365-2958.1997.2311591.X
A cloned pathogenicity island from enteropathogenic Escherichia coli confers the attaching and effacing phenotype on E. coli K‐12
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TL;DR: Cloned a 35.4 kb ‘pathogenicity island’ from the prototype AE bacterium, enteropathogenic Escherichia coli, containing all previously described AE genes, demonstrating that the defining feature of this class of pathogens can be acquired by an avirulent bacterium in a single genetic step.
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Abstract: Attaching and effacing (AE) bacteria are a diverse group of gastrointestinal pathogens, comprising members of four genera, that cause the intestinal epithelial microvilli to be replaced with raised clusters of filamentous actin that conform to the surface of attached bacteria. We have cloned a 35.4 kb ‘pathogenicity island’ from the prototype AE bacterium, enteropathogenic Escherichia coli, containing all previously described AE genes. Transfer of this pathogenicity island to avirulent E. coli converts the recipients into strains that secrete virulence proteins, induce host signal-transduction pathways, and cause AE lesions on cultured epithelial cells. These results demonstrate that this pathogenicity island contains all pathogen-specific genes necessary for inducing AE lesions, and that the defining feature of this class of pathogens can be acquired by an avirulent bacterium in a single genetic step.
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Citations
Role of Escherichia coli O157:H7 Virulence Factors in Colonization at the Bovine Terminal Rectal Mucosa
TL;DR: Virulence factors important for the clinical manifestations of human E. coli O157:H7 infection are analyzed and patterns consistently predicted long-term colonization or clearance of the bacteria from the bovine terminal rectal mucosa.
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A novel proline-rich protein, EspF, is secreted from enteropathogenic Escherichia coli via the type III export pathway
TL;DR: A proline-rich protein, EspF, encoded by the LEE that is secreted by the EPEC type III secretion apparatus is described and surprisingly it retains the ability to induce host signaling events, perform A/E activities, and invade host epithelial cells.
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Insertion of EspD into epithelial target cell membranes by infecting enteropathogenic Escherichia coli.
TL;DR: It is proposed that the membrane‐located EspD protein is part of the translocation apparatus for Esp proteins into the target host cell performing functions similar to YopB in Yersinia.
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Mice Lacking T and B Lymphocytes Develop Transient Colitis and Crypt Hyperplasia yet Suffer Impaired Bacterial Clearance during Citrobacter rodentium Infection
TL;DR: Surprisingly, despite remaining heavily infected, tissues from RAG1 KO mice surviving the acute colitis showed few signs of disease and emphasize the important contribution of the host immune response during infection by A/E bacterial pathogens.
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An activator of glutamate decarboxylase genes regulates the expression of enteropathogenic Escherichia coli virulence genes through control of the plasmid-encoded regulator, Per.
Sooan Shin,Marie-Pierre Castanie-Cornet,John W. Foster,J. Adam Crawford,Carl Brinkley,James B. Kaper +5 more
TL;DR: GadX may be involved in the appropriate expression of genes required for acid resistance and virulence of EPEC, consistent with a model in which environmental changes resulting from passage from the stomach to the proximal small intestine induce the functional effect of GadX on per and GAD expression in order to prevent inappropriate expression of the products of these two systems.
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References
A genetic locus of enterocyte effacement conserved among diverse enterobacterial pathogens.
TL;DR: It is reported that in EPEC a 35-kbp locus containing several regions implicated in formation of these lesions is found, which hybridize to E. coli O157:H7 and other pathogens of three genera that cause similar lesions but do not hybridized to avirulent members of the same species.
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A genetic locus of enteropathogenic Escherichia coli necessary for the production of attaching and effacing lesions on tissue culture cells.
TL;DR: The ability of enteropathogenic Escherichia coli to form attaching and effacing intestinal lesions is a major characteristic of EPEC pathogenesis and a chromosomal gene (eae) that is necessary for this activity is identified using TnphoA mutagenesis.
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Attaching and effacing activities of rabbit and human enteropathogenic Escherichia coli in pig and rabbit intestines.
TL;DR: Three strains of enteropathogenic Escherichia coli (EPEC), originally isolated from humans and previously shown to cause diarrhea in human volunteers by unknown mechanisms, and one rabbit EPEC strain were shown to attach intimately to and efface microvilli and cytoplasm from intestinal epithelial cells in both the pig and rabbit intestine.
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Enteropathogenic Escherichia coli contains a putative type III secretion system necessary for the export of proteins involved in attaching and effacing lesion formation
Karen G. Jarvis,Jorge A. Girón,Ann E. Jerse,Timothy K. McDaniel,Michael S. Donnenberg,James B. Kaper +5 more
TL;DR: The identified EPEC chromosomal genes whose predicted protein sequences are similar to components of a recently described secretory pathway (type III) responsible for exporting proteins lacking a typical signal sequence suggest that the EPEC Sep proteins are component of a type III secretory apparatus necessary for the export of virulence determinants.
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Helicobacter pylori attachment to gastric cells induces cytoskeletal rearrangements and tyrosine phosphorylation of host cell proteins
TL;DR: Results indicate that attachment of H. pylori to gastric epithelial cells resembles that of enteropathogenic Escherichia coli, and cytoskeletal components actin, alpha-actinin, and talin are involved in the process.
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