Oxidative Stress in Shiga Toxin Production by Enterohemorrhagic Escherichia coli

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.

Influence of SOS-inducing agents on the expression of ArtAB toxin gene in Salmonella enterica and Salmonella bongori

“…Previously, we reported that H 2 O 2 also induced ArtAB production in S. Typhimurium DT104 [9]. [15,16,[31][32][33]. In E. coli treated with H 2 O 2 , only a very small fraction of cells is induced for prophage excision and subsequent lytic development, compared to cells treated with MTC [15,31].…”

“…Absence of cI leads to the expression of the anti-terminators Q. The protein Q allows read-through of terminators that inhibit transcription of late phage genes, including stxAB, which is located between Q and Holin genes [15,28]. The ArtAB-encoding genes of S. Typhimurium DT104 strain U1 and S. Worthington strain 182 share the location of stx2 within a functional prophage (Y. Tamamura, I. Uchida, M. Akiba and M. Kusumoto, unpublished data).…”

“…Shiga toxin production in Escherichia coli is coregulated through induction of the prophage that encodes toxin gene stx2 [11][12][13][14][15][16][17][18]. Activation of the SOS response by MTC and H 2 O 2 , which cause DNA damage, or antimicrobial agents such as quinolones, which inhibit DNA replication, triggers substantial Stx-phage induction and results in high Stx2 production [11][12][13][14][15][16][17]19]. Since the effect of H 2 O 2 or antibiotics on ArtAB production in Salmonella spp.…”

Role of orf73 in the development of lambdoid bacteriophages during infection of the Escherichia coli host

“…Under such conditions, the RecA protein recognizes bacterial single-stranded DNA fragments and is activated to stimulate the self-cleavage of the cI repressor. This leads to initiation of phage lytic cycle through transcription from the early p L and p R promoters (Łoś et al, 2009;Węgrzyn et al, 2012;Szych et al, 2013;Licznerska et al, 2016a).…”

<b> Antibacterial activity of Aroeira honeys produced in Minas-Gerais against bacteria of clinical importance

“…Enterohemorrhagic E. coli (EHEC) is a pathogenic E. coli line capable of causing disease in humans and is responsible for a large number of food-borne diseases associated with outbreaks of bloody diarrhea, which may be complicated by the development of hemolytic uremic syndrome (HUS) (Jost, Bidet, Carrère, Kurkdjian, & Bonacorsi, 2016). Antimicrobial therapy is not recommended during EHEC infection because of the risk of developing HUS through the induction and/or production of Shiga toxin, the main virulence factor of EHEC (Licznerska, et al, 2016).…”