Oxidative Stress in Shiga Toxin Production by Enterohemorrhagic Escherichia coli

Oxid Med Cell Longev. 2016;2016:3578368. doi: 10.1155/2016/3578368. Epub 2015 Dec 20.

Abstract

Virulence of enterohemorrhagic Escherichia coli (EHEC) strains depends on production of Shiga toxins. These toxins are encoded in genomes of lambdoid bacteriophages (Shiga toxin-converting phages), present in EHEC cells as prophages. The genes coding for Shiga toxins are silent in lysogenic bacteria, and prophage induction is necessary for their efficient expression and toxin production. Under laboratory conditions, treatment with UV light or antibiotics interfering with DNA replication are commonly used to induce lambdoid prophages. Since such conditions are unlikely to occur in human intestine, various research groups searched for other factors or agents that might induce Shiga toxin-converting prophages. Among other conditions, it was reported that treatment with H2O2 caused induction of these prophages, though with efficiency significantly lower relative to UV-irradiation or mitomycin C treatment. A molecular mechanism of this phenomenon has been proposed. It appears that the oxidative stress represents natural conditions provoking induction of Shiga toxin-converting prophages as a consequence of H2O2 excretion by either neutrophils in infected humans or protist predators outside human body. Finally, the recently proposed biological role of Shiga toxin production is described in this paper, and the "bacterial altruism" and "Trojan Horse" hypotheses, which are connected to the oxidative stress, are discussed.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Enterohemorrhagic Escherichia coli / metabolism*
  • Humans
  • Hydrogen Peroxide / metabolism
  • Oxidative Stress*
  • Prophages / metabolism
  • Shiga Toxin / biosynthesis*

Substances

  • Shiga Toxin
  • Hydrogen Peroxide