Abstract

Pathogenicity of enterohemorrhagic Escherichia coli (EHEC) strains depends on various virulence factors, like adhesins (including intimin), flagella, type I fimbriae, curli fibers, hemolysins, and agents required for biofilm formation. However, the pathogenicity is highly enhanced by production of Shiga toxins which are encoded by stx genes located in genomes of Shiga toxin-converting (Stx) prophages. Thus, for maximal EHEC virulence, induction of these prophages is necessary. Although various physical and chemical agents causing Stx prophage induction are known, it is not clear whether any food can stimulate this process. Therefore, the aim of this work was to test whether commonly used drinks might enhance Stx prophage induction in E. coli. It was found that 5% Nestea, but not 5% Coca-Cola or 1% ethanol, caused a significant induction of 933W Stx prophage in a bacterial culture in vitro. These results indicate that some commonly used drinks can stimulate Stx prophage induction, potentially enhancing virulence of EHEC. This may have impact on protection of consumers which are infected by these bacteria, and might contribute to choose safe food for such persons.

Highlights

  • Pathogenicity of enterohemorrhagic Escherichia coli (EHEC) strains depends on various virulence factors, like adhesins, flagella, type I fimbriae, curli fibers, hemolysins, and agents required for biofilm formation

  • The pathogenicity is highly enhanced by production of Shiga toxins which are encoded by stx genes located in genomes of Shiga toxin-converting (Stx) prophages

  • Vast majority of Escherichia coli strains are harmless to humans, and they occur as a part of natural microbiota in the human gut

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Summary

Introduction

Vast majority of Escherichia coli strains are harmless to humans, and they occur as a part of natural microbiota in the human gut. The aim of this work was to test whether commonly used drinks might enhance Stx prophage induction in E. coli. It was found that 5% Nestea, but not 5% Coca-Cola or 1% ethanol, caused a significant induction of 933W Stx prophage in a bacterial culture in vitro.

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