Global Expression of Prophage Genes in
            <i>Escherichia coli</i>
            O157:H7 Strain EDL933 in Response to Norfloxacin

Herold, Sylvia; Siebert, Jutta; Huber, Andrea; Schmidt, Herbert

doi:10.1128/aac.49.3.931-944.2005

Cited by 83 publications

(73 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In accordance with other authors (20), we hypothesized that the expression of phage genes may be regulated when other temperate phages are present. We examined in an E. coli K-12 background the effect on phage and toxin production when the same host strain was converted by one or two Stx prophages.…”

supporting

confidence: 54%

The CI Repressors of Shiga Toxin-Converting Prophages Are Involved in Coinfection of Escherichia coli Strains, Which Causes a Down Regulation in the Production of Shiga Toxin 2

2008

View full text Add to dashboard Cite

Shiga toxins (Stx) are the main virulence factors associated with a form of Escherichia coli known as Shiga toxin-producing E. coli (STEC). They are encoded in temperate lambdoid phages located on the chromosome of STEC. STEC strains can carry more than one prophage. Consequently, toxin and phage production might be influenced by the presence of more than one Stx prophage on the bacterial chromosome. To examine the effect of the number of prophages on Stx production, we produced E. coli K-12 strains carrying either one Stx2 prophage or two different Stx2 prophages. We used recombinant phages in which an antibiotic resistance gene (aph, cat, or tet) was incorporated in the middle of the Shiga toxin operon. Shiga toxin was quantified by immunoassay and by cytotoxicity assay on Vero cells (50% cytotoxic dose). When two prophages were inserted in the host chromosome, Shiga toxin production and the rate of lytic cycle activation fell. The cI repressor seems to be involved in incorporation of the second prophage. Incorporation and establishment of the lysogenic state of the two prophages, which lowers toxin production, could be regulated by the CI repressors of both prophages operating in trans. Although the sequences of the cI genes of the phages studied differed, the CI protein conformation was conserved. Results indicate that the presence of more than one prophage in the host chromosome could be regarded as a mechanism to allow genetic retention in the cell, by reducing the activation of lytic cycle and hence the pathogenicity of the strains.

show abstract

supporting

confidence: 54%

The CI Repressors of Shiga Toxin-Converting Prophages Are Involved in Coinfection of Escherichia coli Strains, Which Causes a Down Regulation in the Production of Shiga Toxin 2

2008

View full text Add to dashboard Cite

show abstract

“…Effectively, in a study that investigated global gene expression during growth transitions of E. coli O157:H7, the transcript levels of stx2A decreased 1.5-fold from late exponential to stationary phase, while levels of stx2B remained higher in stationary phase than in exponential phase (5). In contrast, when global expression of EDL933 in response to norfloxacin was obtained, the transcript levels of stx2A were at least twice as high as those of stx2B (25).…”

Section: Discussionmentioning

confidence: 99%

Escherichia coliO157:H7 Survives within Human Macrophages: Global Gene Expression Profile and Involvement of the Shiga Toxins

et al. 2008

View full text Add to dashboard Cite

Escherichia coli O157:H7 is an important food-borne pathogen that specifically binds to the follicle-associated epithelium in the intestine, which rapidly brings this bacterial pathogen in contact with underlying human macrophages. Very little information is available about the interaction between E. coli O157:H7 and human macrophages. We evaluated the uptake and survival of strain EDL933 during infection of human macrophages. Surprisingly, EDL933 survived and multiplied in human macrophages at 24 h postinfection. The global gene expression profile of this pathogen during macrophage infection was determined. Inside human macrophages, upregulation of E. coli O157:H7 genes carried on O islands (such as pagC, the genes for both of the Shiga toxins, and the two iron transport system operons fit and chu) was observed. Genes involved in acid resistance and in the SOS response were upregulated. However, genes of the locus of enterocyte effacement or genes involved in peroxide resistance were not differentially expressed. Many genes with putative or unknown functions were upregulated inside human macrophages and may be newly discovered virulence factors. As the Shiga toxin genes were upregulated in macrophages, survival and cytotoxicity assays were performed with isogenic Shiga toxin mutants. The initial uptake of Shiga toxins mutants was higher than that of the wild type; however, the survival rates were significantly lower at 24 h postinfection. Thus, Shiga toxins are implicated in the interaction between E. coli O157:H7 and human macrophages. Understanding the molecular mechanisms used by E. coli to survive within macrophages may help in the identification of targets for new therapeutic agents.Enterohemorragic Escherichia coli (EHEC) causes an acute gastroenteritis, bloody diarrhea, and hemorrhagic colitis. Severe complications develop in up to 10% of cases, including the hemolytic-uremic syndrome, which can be fatal (45,56). EHEC strains share their genetic backbone with the laboratory strain K-12 and also contain 1.34 Mb of extra genetic material called O islands (OI) (46). In the EHEC strain EDL933 (O157: H7), 177 OI were identified; some of them harbor genes for important known virulence factors of EHEC, such as the locus of enterocyte effacement (LEE) and two different Shiga toxins, Stx1 and Stx2. Following the ingestion of contaminated food or water, EHEC enters the gastrointestinal tract, survives the acidic conditions of the stomach, and is released in the intestine. Adhesion of the bacteria to the intestinal wall is the first step in establishing infection. The LEE encodes a type III secretion system (T3SS) that injects effectors in host epithelial cells, creating an intimate binding, involving actin rearrangement and microvillus effacement, which results in the pathological lesions called attaching and effacing lesions (40, 52). In the large intestine, EHEC specifically adheres to the follicleassociated epithelium of Peyer's patches (47). Binding at the follicle-associated epithelium results in the rapid co...

show abstract

“…The effect of a sub-inhibitory concentration against environmental bacteria is still unknown. It was reported that FQs at concentrations 10-100 times weaker than the MIC induced the expression of a functional gene (16), mutations (11), and morphological changes (33) at the single cell level. The concentrations detected in this study were lower than those.…”

Section: Discussionmentioning

confidence: 99%

Fluoroquinolone (FQ) Contamination Does Not Correlate with Occurrence of FQ-Resistant Bacteria in Aquatic Environments of Vietnam and Thailand

et al. 2011

View full text Add to dashboard Cite

Fluoroquinolone antibiotics (FQs) have been used worldwide for chemotherapy, animal husbandry, and aquaculture, and the occurrence of FQ-resistant (FQs r ) bacteria in natural environments has been reported. Plasmid-mediated transferable quinolone resistance (PMQR) genes are suspected to originate from the chromosomes of water-dwelling bacteria. However, the occurrence of and the potential reservoir of FQs r bacteria and PMQR genes in aquatic environments have not been elucidated. In this study, we detected FQs r bacteria and PMQR genes in aquatic environments in Thailand and Vietnam, and measured FQ contamination. Levels of contamination were greater Thailand (avg. 5130, max 46100 ng L −1 ) than in Vietnam (avg. 235, max 1130 ng L −1 ); however, the occurrence of FQs r bacteria was higher in Vietnam (~15%) than in Thailand (~7.0%), suggesting that contamination by FQs is not directly linked to the development of FQs r bacteria. Diverse taxonomic groups of FQs r -bacteria were identified, and one of the PMQR genes, qnrB, was detected from bacteria of environmental origin, not enteric bacteria. This suggests that the environmental bacteria are a potential reservoir of antibiotic resistance determinants even at un-contaminated sites.

show abstract

Global Expression of Prophage Genes in Escherichia coli O157:H7 Strain EDL933 in Response to Norfloxacin

Cited by 83 publications

References 57 publications

The CI Repressors of Shiga Toxin-Converting Prophages Are Involved in Coinfection of Escherichia coli Strains, Which Causes a Down Regulation in the Production of Shiga Toxin 2

The CI Repressors of Shiga Toxin-Converting Prophages Are Involved in Coinfection of Escherichia coli Strains, Which Causes a Down Regulation in the Production of Shiga Toxin 2

Escherichia coliO157:H7 Survives within Human Macrophages: Global Gene Expression Profile and Involvement of the Shiga Toxins

Fluoroquinolone (FQ) Contamination Does Not Correlate with Occurrence of FQ-Resistant Bacteria in Aquatic Environments of Vietnam and Thailand

Contact Info

Product

Resources

About