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Sylvia Kleta

Researcher at Free University of Berlin

Publications -  7
Citations -  558

Sylvia Kleta is an academic researcher from Free University of Berlin. The author has contributed to research in topics: Escherichia coli & Population. The author has an hindex of 5, co-authored 5 publications receiving 500 citations. Previous affiliations of Sylvia Kleta include Federal Institute for Risk Assessment.

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Characterization of a porcine intestinal epithelial cell line for in vitro studies of microbial pathogenesis in swine

TL;DR: The permanent porcine intestinal epithelial cell line, IPEC-J2, is characterized using a variety of methods to assess the usefulness of this cell line as an in vitro infection model and concludes that it provides a relevant in vitro model system for porCine intestinal pathogen–host cell interactions.
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Virulence Factor Gene Profiles of Escherichia coli Isolates from Clinically Healthy Pigs

TL;DR: The results appear to indicate that virulence gene-carrying E. coli strains are a normal part of intestinal bacterial populations and that high numbers of E. Escherichia coli cells harboring virulence genes and/or with hemolytic activity do not necessarily correlate with disease.
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Detection and distribution of probiotic Escherichia coli Nissle 1917 clones in swine herds in Germany

TL;DR: To verify the presence of Escherichia coli Nissle 1917 as a natural isolate in swine and to characterize in vitro probiotic properties as well as in vivo persistence in a feeding experiment.
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E. coli Nissle 1917 Affects Salmonella Adhesion to Porcine Intestinal Epithelial Cells

TL;DR: It is proposed that EcN affects Salmonella adhesion through secretory components, which appears to be common to many E. coli strains, with strong adherence being a prerequisite for an effective reduction of SiiE-mediated Salmoneella adhesion.
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Role of F1C Fimbriae, Flagella, and Secreted Bacterial Components in the Inhibitory Effect of Probiotic Escherichia coli Nissle 1917 on Atypical Enteropathogenic E. coli Infection

TL;DR: It is proposed that the strong adhesion capacities enable EcN to secrete sufficient local concentrations of the inhibitory factors to reduce the infection efficiencies of aEPEC by inhibiting bacterial adhesion and growth of microcolonies, but not the attaching and effacing of adherent bacteria.