scholarly journals Oxidative Stress in Shiga Toxin Production by EnterohemorrhagicEscherichia coli

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Katarzyna Licznerska ◽  
Bożena Nejman-Faleńczyk ◽  
Sylwia Bloch ◽  
Aleksandra Dydecka ◽  
Gracja Topka ◽  
...  

Virulence of enterohemorrhagicEscherichia 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 H2O2caused 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 H2O2excretion 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.

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Katarzyna Licznerska ◽  
Aleksandra Dydecka ◽  
Sylwia Bloch ◽  
Gracja Topka ◽  
Bożena Nejman-Faleńczyk ◽  
...  

Previous studies indicated that these genetic elements could be involved in the regulation of lysogenization and prophage induction processes. The effects were dramatic in Shiga toxin-converting phageΦ24Bafter treatment with oxidative stress-inducing agent, hydrogen peroxide, while they were less pronounced in bacteriophageλand in both phages irradiated with UV. The hydrogen peroxide-caused prophage induction was found to be RecA-dependent. Importantly, in hydrogen peroxide-treatedE. colicells lysogenic for eitherλorΦ24B, deletion of theexo-xisregion resulted in a significant decrease in the levels of expression of the S.O.S. regulon genes. Moreover, under these conditions, a dramatic decrease in the levels of expression of phage genes crucial for lytic development (particularlyxis, exo, N, cro, O, Q, andR) could be observed inΦ24B-, but not inλ-bearing cells. We conclude that genes located in theexo-xisregion are necessary for efficient expression of both host S.O.S regulon in lysogenic bacteria and regulatory genes of Shiga toxin-converting bacteriophageΦ24B.


Author(s):  
Su-bin Hwang ◽  
Ramachandran Chelliah ◽  
Ji Eun Kang ◽  
Momna Rubab ◽  
Eric Banan-MwineDaliri ◽  
...  

Shiga toxin-producing Escherichia coli (STEC) is a global foodborne bacterial pathogen that is often accountable for colon disorder or distress. STEC commonly induces severe diarrhea in hosts but can cause critical illnesses due to the Shiga toxin virulence factors. To date, there have been a significant number of STEC serotypes have been evolved. STECs vary from nausea and hemorrhoid (HC) to possible lethal hemolytic-based uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP). Inflammation-based STEC is usually a foodborne illness with Shiga toxins (Stx 1 and 2) thought to be pathogenesis. The STEC’s pathogenicity depends significantly on developing one or more Shiga toxins, which can constrain host cell protein synthesis leading to cytotoxicity. In managing STEC infections, antimicrobial agents are generally avoided, as bacterial damage and discharge of accumulated toxins are thought the body. It has also been documented that certain antibiotics improve toxin production and the development of these species. Many different groups have attempted various therapies, including toxin-focused antibodies, toxin-based polymers, synbiotic agents, and secondary metabolites remedies. Besides, in recent years, antibiotics’ efficacy in treating STEC infections has been reassessed with some encouraging methods. Nevertheless, the primary role of synbiotic effectiveness (probiotic and prebiotic) against pathogenic STEC and other enteropathogens is less recognized. Additional studies are required to understand the mechanisms of action of probiotic bacteria and yeast against STEC infection. Because of the consensus contraindication of antimicrobials for these bacterial pathogens, the examination was focused on alternative remedy strategies for STEC infections. The rise of novel STEC serotypes and approaches employed in its treatment are highlighted.


2001 ◽  
Vol 69 (3) ◽  
pp. 1934-1937 ◽  
Author(s):  
Patrick L. Wagner ◽  
David W. K. Acheson ◽  
Matthew K. Waldor

ABSTRACT The Shiga toxins (Stx) are critical virulence factors forEscherichia coli O157:H7 and other serotypes of enterohemorrhagic E. coli (EHEC). These potent toxins are encoded in the genomes of temperate lambdoid bacteriophages. We recently demonstrated that induction of the resident Stx2-encoding prophage in an O157:H7 clinical isolate is required for toxin production by this strain. Since several factors produced by human cells, including hydrogen peroxide (H2O2), are capable of inducing lambdoid prophages, we hypothesized that such molecules might also induce toxin production by EHEC. Here, we studied whether H2O2 and also human neutrophils, an important endogenous source of H2O2, induced Stx2 expression by an EHEC clinical isolate. Both H2O2 and neutrophils were found to augment Stx2 production, raising the possibility that these agents may lead to prophage induction in vivo and thereby contribute to EHEC pathogenesis.


2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Ganna Petruk ◽  
Rita Del Giudice ◽  
Maria Manuela Rigano ◽  
Daria Maria Monti

Exposure to UV light triggers the rapid generation and accumulation of reactive oxygen species (ROS) in skin cells, with consequent increase in oxidative stress and thus in photoaging. Exogenous supplementation with dietary antioxidants and/or skin pretreatment with antioxidant-based lotions before sun exposure might be a winning strategy against age-related skin pathologies. In this context, plants produce many secondary metabolites to protect themselves from UV radiations and these compounds can also protect the skin from photoaging. Phenolic compounds, ascorbic acid and carotenoids, derived from different plant species, are able to protect the skin by preventing UV penetration, reducing inflammation and oxidative stress, and influencing several survival signalling pathways. In this review, we focus our attention on the double role of oxidants in cell metabolism and on environmental and xenobiotic agents involved in skin photoaging. Moreover, we discuss the protective role of dietary antioxidants from fruits and vegetables and report their antiaging properties related to the reduction of oxidative stress pathways.


2018 ◽  
Vol 10 (2) ◽  
pp. 128-32 ◽  
Author(s):  
Mashuri Mashuri ◽  
Mustofa Ruhullah ◽  
Bayu Diertama Putera ◽  
Vicky Pramudinta Mega ◽  
Fadillah Alma Putra ◽  
...  

BACKGROUND: Ceftazidime was known to cause photosensitization reactions. However, how it plays the role remained unclear. In our study, we aim to investigate the photosensitization effect of ceftazidime in erythrocytes via oxidative stress.METHODS: Samples were divided into six different groups: negative control group, positive control group and four experimental groups with 10%, 20%, 30%, and 40% ceftazidime, respectively. The positive control and experimental groups were exposed to ultraviolet (UV)-light for 2 hours. Superoxide radical, malondialdehyde (MDA), carbonyl compounds (CC) and methemoglobin (Met-Hb) levels were then measured.RESULTS: The results showed a significant increased of superoxide radical, MDA, CC and Met-Hb levels in all experimental groups compared to both negative or positive control groups (p< 0.05).CONCLUSION: In conclusion, our study confirmed the role of ceftazidime as a photosensitizer in erythrocytes via the oxidative stress mechanisms.KEYWORDS: ceftazidime, oxidative stress, photosensitizer, photosensitization.


2000 ◽  
Vol 278 (5) ◽  
pp. G811-G819 ◽  
Author(s):  
Nicola L. Jones ◽  
Avinash Islur ◽  
Rizwan Haq ◽  
Mariola Mascarenhas ◽  
Mohamed A. Karmali ◽  
...  

Human intestinal cells lack globotriaosylceramide (Gb3), the receptor for Shiga toxin-1 (Stx1) and Shiga toxin-2 (Stx2). Therefore, the role of these toxins in mediating intestinal disease during infection with Shiga toxin-producing Escherichia coli is unclear. The aims of this study were to determine whether Stx1 and Stx2 induce apoptosis in epithelial cells expressing (HEp-2, Caco-2) or lacking (T84) Gb3and to characterize the role of the Bcl-2 family. Stx1 (12.5 ng/ml) induced apoptosis in both HEp-2 (21.9 ± 7.9% vs. 0.8 ± 0.3%, P = 0.01) and Caco-2 (10.1 ± 1.2% vs. 3.1 ± 0.4%, P = 0.006) cells but not in Gb3-deficient T84 cells. Toxin-mediated apoptosis of HEp-2 cells was associated with enhanced expression of the proapoptotic protein Bax. Inhibition of caspase activation prevented toxin-stimulated apoptosis. In addition, overexpression of Bcl-2 by transient transfection blocked Stx1-stimulated cell death. These findings indicate that Shiga toxins produced by E. coli signal Gb3-expressing epithelial cells to undergo apoptosis in association with enhanced Bax expression, thereby resulting in activation of the caspase cascade.


Antibiotics ◽  
2018 ◽  
Vol 7 (4) ◽  
pp. 101 ◽  
Author(s):  
Cristina Howard-Varona ◽  
Dean Vik ◽  
Natalie Solonenko ◽  
Yueh-Fen Li ◽  
M. Gazitua ◽  
...  

Hemolytic–uremic syndrome is a life-threating disease most often associated with Shiga toxin-producing microorganisms like Escherichia coli (STEC), including E. coli O157:H7. Shiga toxin is encoded by resident prophages present within this bacterium, and both its production and release depend on the induction of Shiga toxin-encoding prophages. Consequently, treatment of STEC infections tend to be largely supportive rather than antibacterial, in part due to concerns about exacerbating such prophage induction. Here we explore STEC O157:H7 prophage induction in vitro as it pertains to phage therapy—the application of bacteriophages as antibacterial agents to treat bacterial infections—to curtail prophage induction events, while also reducing STEC O157:H7 presence. We observed that cultures treated with strictly lytic phages, despite being lysed, produce substantially fewer Shiga toxin-encoding temperate-phage virions than untreated STEC controls. We therefore suggest that phage therapy could have utility as a prophylactic treatment of individuals suspected of having been recently exposed to STEC, especially if prophage induction and by extension Shiga toxin production is not exacerbated.


2001 ◽  
Vol 183 (6) ◽  
pp. 2081-2085 ◽  
Author(s):  
Patrick L. Wagner ◽  
Melody N. Neely ◽  
Xiaoping Zhang ◽  
David W. K. Acheson ◽  
Matthew K. Waldor ◽  
...  

ABSTRACT Shiga toxins (Stxs), encoded by the stxA andstxB genes, are important contributors to the virulence ofEscherichia coli O157:H7 and other Stx-producing E. coli (STEC) strains. The stxA and stxBgenes in STEC strains are located on the genomes of resident prophages of the λ family immediately downstream of the phage late promoters (p R′). The phage-encoded Q proteins modify RNA polymerase initiating transcription at the cognatep R′ promoter which creates transcription complexes that transcend a transcription terminator immediately downstream of p R′ as well as terminator kilobases distal to p R′. To test if this Q-directed processive transcription plays a role instx 2 AB expression, we constructed a mutant prophage in an O157:H7 clinical isolate from whichp R′ and part of Q were deleted but which has an intact pStx, the previously describedstx 2 AB-associated promoter. We report that production of significant levels of Stx2 in this O157:H7 isolate depends on the p R′ promoter. Since transcription initiating at p R′ ultimately requires activation of the phage lytic cascade, expression ofstx 2 AB in STEC depends primarily on prophage induction. By showing this central role for the prophage instx 2 AB expression, our findings contradict the prevailing assumption that phages serve merely as agents for virulence gene transfer.


2008 ◽  
Vol 7 (6) ◽  
pp. 988-1000 ◽  
Author(s):  
Massimo Reverberi ◽  
Slaven Zjalic ◽  
Alessandra Ricelli ◽  
Federico Punelli ◽  
Emanuela Camera ◽  
...  

ABSTRACT Oxidative stress is recognized as a trigger of different metabolic events in all organisms. Various factors correlated with oxidation, such as the β-oxidation of fatty acids and their enzymatic or nonenzymatic by-products (e.g., precocious sexual inducer factors and lipoperoxides) have been shown to be involved in aflatoxin formation. In the present study, we found that increased levels of reactive oxygen species (ROS) were correlated with increased levels of aflatoxin biosynthesis in Aspergillus parasiticus. To better understand the role of ROS formation in toxin production, we generated a mutant (ΔApyapA) having the ApyapA gene deleted, given that ApyapA orthologs have been shown to be part of the antioxidant response in other fungi. Compared to the wild type, the mutant showed an increased susceptibility to extracellular oxidants, as well as precocious ROS formation and aflatoxin biosynthesis. Genetic complementation of the ΔApyapA mutant restored the timing and quantity of toxin biosynthesis to the levels found in the wild type. The presence of putative AP1 (ApYapA orthologue) binding sites in the promoter region of the regulatory gene aflR further supports the finding that ApYapA plays a role in the regulation of aflatoxin biosynthesis. Overall, our results show that the lack of ApyapA leads to an increase in oxidative stress, premature conidiogenesis, and aflatoxin biosynthesis.


Author(s):  
Karolina Zdrojewska ◽  
Aleksandra Dydecka ◽  
Bożena Nejman-Faleńczyk ◽  
Gracja Topka ◽  
Agnieszka Necel ◽  
...  

Shiga toxin-producing Escherichia coli (STEC) is a group of pathogenic strains responsible for human infections that result in bloody diarrhea and hemorrhagic colitis, often with severe complications. The main virulence factors of STEC are Shiga toxins encoded by stx genes located in genomes of Shiga toxin-converting bacteriophages (Stx phages). These bacterial viruses are clustered in the lambdoid bacteriophages family represented by phage λ. Here, we report that expression of orf73 from the exo-xis region of the phage genome promotes the lysogenic pathway of development of λ and Φ24B phages. We demonstrated that the mutant phages with deletions of orf73 revealed higher burst size during the lytic cycle. Moreover, survival rates of E. coli infected with mutant bacteriophages were lower relative to wild-type viruses. Additionally, orf73 deletion negatively influenced the lysogenization process of E. coli host cells. We conclude that orf73 plays an important biological role in the development of lambdoid viruses, and probably it is involved in the network of molecular mechanism of the lysis-vs.-lysogenization decision.


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