Dissertations / Theses: 'Verotoxine'

1

Assmus, Nadine. "Antibiotika-Resistenzen bei Verotoxin-bildenden Escherichia coli-Stämmen, isoliert aus Kot- und Lebensmittelproben der Tierart Rind." Giessen VVB Laufersweiler, 2009. http://d-nb.info/996010009/04.

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2

Delorme, Sandrine. "Untersuchungen zum Nachweis von verotoxinogenen E.coli (VTEC), speziell Serovar O157, in Lebensmitteln tierischen Ursprungs mit verschiedenen Anreicherungsverfahren /." Giessen : VVB Laufersweiler, 2008. http://d-nb.info/991416341/04.

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3

Delorme, Sandrine. "Untersuchungen zum Nachweis von verotoxinogenen E. coli (VTEC), speziell Serovar O157, in Lebensmitteln tierischen Ursprungs mit verschiedenen Anreicherungsverfahren." Giessen : VVB Laufersweiler, 2008. http://d-nb.info/991918991/34.

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4

Urabi, Iftikhar. "Virulence factors of verotoxin-producing Escherichia coli O157:H7." Thesis, University of Warwick, 1993. http://wrap.warwick.ac.uk/104210/.

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Escherichia coli O157:H7 is one of several E.coli serotypes that produce Verocytotoxins (VTs); they are collectively called "Verocytotoxin-producing E.coli" (VTEC). VTEC are medically important bacteria which have been implicated in cases of haemorrhagic colitis and haemolytic uremic syndrome. Two distinct VTs are known, VT1 and VT2, and variants of VT2 have been described. They are potent exotoxins which kill mammalian cells by inhibiting protein synthesis. The virulence properties manifested by these organisms include the elaboration of VT1 or VT2 (or both), and the adherence to intestinal epithelial cells via an attaching-effacing mechanism. Many strains carry a 60 MDa plasmid which is thought to be involved in adhesion. Initial data demonstrated that the VTEC O157:H7 isolates under study possess two virulence factors, production of VTs and adherence to epithelial cells. However, effort has focused on investigating bacterial adherence, largely because attachment of VTEC is thought to be an important pathogenic mechanism since it allows colonisation, which facilitates toxin delivery, and adherence may be sufficient to cause diarrhoea in experimental animals in the absence of VTs. Moreover, a better understanding of the adhesion mechanism should help in finding ways by which adherence can be prevented. Since the bacterial-mucosal interactions are complicated in vivo by events and conditions that are not reproduced in current in vitro tests, a series of experiments were designed to investigate bacterial adherence to epithelial cells under conditions which are as close as possible to the in vivo situation. Significantly different data were obtained when quantitative adherence assays were performed under different physiological conditions, (different growth media, growth phase, pH values, low iron and oxygen limitation). Both iron-restricted, and oxygen- limited media induced a reduction in the final cell density, however, anaerobiosis significantly increased the adherence capacity of VTEC O157:H7 to HeLa cells while low iron caused a reduction in the number of adherent bacteria. Actively growing cells in the exponential phase were more adherent to HeLa cells than cells in the stationary phase. Since adhesion results from mutual recognition of surface structures from both the bacterial cell (adhesin) and the host cell (receptor), the bacterial cell envelope, and the HeLa cell outer membranes were investigated. Results of the preliminary characterisation of VTEC 0157:H7 surface components which have been implicated as adherence factors indicated that these strains are not fimbriated, however, they have been shown to be capable of binding to epithelial cells. Further studies were therefore, focused upon the identification of nonfimbrial adhesin(s). The use of competitive inhibitors, such as bacterial outer membrane extracts (OMPs), isolated lipopolysaccharides (LPS) and rabbit antisera to the H-7 flagella, OMPs, and LPS suggested that the role of H-7 flagella is insignificant, the LPS may in part be involved, but the OMPs seemed to have the major role in mediating attachment of O157:H7 to HeLa cells. The expression of OMPs under variable cultural conditions was examined, and significant differences were detected by the SDS-PAGE analysis of these extracts. The expression and repression of certain proteins was apparent under anaerobiosis, iron-restriction, different pH values and different bacterial growth phases. HeLa cell outer membranes were studied to identify the receptors on the host cell. Purified outer membranes were analysed by SDS-PAGE and used as inhibitors of bacterial adherence. Two proteins were identified by immunoblotting as a potential receptors.

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5

Ownis, Ali A. "Verocytotoxin expression by E. coli O157:H7." Thesis, University of Warwick, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343149.

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6

Carter, Shanen L. "Production of a human monoclonal antibody reactive against verotoxin-1." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ33946.pdf.

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7

Khandaker, MD Shahjahan Ali. "Economic analysis of diseases caused by VTEC (verotoxin producing e.coli) in Australia /." St. Lucia, Qld, 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17335.pdf.

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8

Arab, Sara. "Studies of the antineoplastic activity of verotoxin in vitro and in vivo." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ27869.pdf.

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9

Dahlfors, Rebecka. "Occurrence of Verotoxin-encoding phages in mussels grown downstream the sewage treatment plant in Lysekil." Thesis, Uppsala University, Department of Medical Biochemistry and Microbiology, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-108306.

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The purpose of this study was to investigate the occurrence of Verotoxin-encoding bacteriophages in mussels, cultured downstream the sewage treatment plant in Lysekil.

Mussels were collected in three growing areas from April 2008 to March 2009. Real-time PCR was performed for detection of vtx1 and vtx2 genes and enrichment of bacteriophages on non Verotoxin-producing Escherichia coli O157: H7 was carried out. All samples in real-time PCR analysis were negative; no presence of Verotoxin-encoding phages was shown. No plaque was formed on blood agar base plates, indicating that no bacteriophages had been taken up by E. coli bacteria

The levels of Verotoxin-encoding phages and E.coli outside the sewage treatment plant in Lysekil were not high enough to be able to form VTEC in mussels, indicating that the faecal contamination was low. This does not exclude the presence of other more common pathogens such as norovirus and campylobacter.

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10

Booth, Ronald A. "Development of cloth-enzyme immunoassays for the detection of E. coli O157 and verotoxin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq22137.pdf.

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11

Booth, Ronald A. Carleton University Dissertation Biology. "Development of cloth-enzyme immunoassays for the detection of E. coli O157 and verotoxin." Ottawa, 1996.

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12

Weinz, Fanny. "Behandling av cisplatinresistent lungcancer : Induktionsstudie av Gb3-uttryck hos lungcancerceller." Thesis, Umeå universitet, Biomedicinsk laboratorievetenskap, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-57975.

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13

Bartels, Andrea Christine [Verfasser]. "Untersuchungen zum Vorkommen von Verotoxin-bildenden Escherichia coli (VTEC) bei Rehwild in Hessen / Andrea Christine Bartels." Gießen : Universitätsbibliothek, 2014. http://d-nb.info/1068589205/34.

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14

Chapman, Peter Alan. "Purification of the verotoxins of Escherichia coli and production of antitoxins for use in a diagnostic test." Thesis, University of Sheffield, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244433.

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15

Aßmus, Nadine [Verfasser]. "Antibiotika-Resistenzen bei Verotoxin-bildenden Escherichia-coli-Stämmen, isoliert aus Kot- und Lebensmittelproben der Tierart Rind / eingereicht von Nadine Aßmus." Giessen : VVB Laufersweiler, 2009. http://d-nb.info/99711827X/34.

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16

Wolski, Winicjusz M. "The three potential glycolipid binding sites of the Verotoxin 1 B subunit, their function in toxicity induction and cytokine release." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0005/MQ46052.pdf.

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17

Bast, Darrin James. "Three biologically significant globotriasylceramide binding sites on the Verotoxin 1 B subunit, implications in toxin action, pathogenesis of disease and vaccine design." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ35106.pdf.

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18

Flagler, Michael J. "Determination of the Molecular Basis for the Difference in Potency between Shiga Toxins 1 and 2." Cincinnati, Ohio : University of Cincinnati, 2010. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1267131436.

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Thesis (Ph.D.)--University of Cincinnati, 2010.
Advisor: Alison A. Weiss. Title from electronic thesis title page (viewed Apr. 26, 2010). Keywords: Shiga toxin; Shiga-like toxin; Verotoxin; Verocytotoxin; B-subunit; B-pentamer. Includes abstract. Includes bibliographical references.

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19

Hamuel, James Doughari. "Effect of stress, antibiotics and phytochemicals on verotoxic isolates of acinetobacter haemolyticus and escherichia coli obtained from water and wastewater samples." Thesis, Cape Peninsula University of Technology, 2012. http://hdl.handle.net/20.500.11838/808.

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Thesis submitted in fulfillment for the requirements for the degree Doctor Technologiae: Environmental Health in the Faculty of Applied Sciences, Cape Peninsula University of Technology, 2012
Water related issues such as water treatment and distribution have become extremely important all over the world due to population growth, growing urbanization, health and environmental pollutions. Contamination of water bodies especially in Africa with antibiotic resistant bacteria strains is a cause for concern. Escherichia coli O157 H:7, and various strains of non O157 E. coli and Acinetobacter spp. are known for antibiotic resistance. Both bacteria are environmental organisms found coexisting together with high potentials of exchange of resistance genes. Despite the stress conditions confronting these bacteria in water, food and the human body, in the form of disinfectants, antibiotics, salts and the innate immunity, they appear to develop adaptive mechanisms that enable them survive and cause infection. This therefore necessitates the need for investigation of effective virulence factor-targeted control measures. Culture of 62 water samples on Brilliance E. coli/coliform selective medium (BECSM, Oxoid), Eosin Methylene Blue (EMB) agar, or Baumann’s enrichment medium (BEM) and Leeds Acinetobacter Medium (LAM) for the isolation of E. coli and Acinetobacter spp. was carried out. Isolates were investigated for virulence factors, antibiotic resistance and transformation of resistance genes. The effect of oxidative stress exerted by 0.3% Crystal violet, 0.3% Bile salt, 4.0% NaCl, and 8% ethanol on some of the multi-drug resistant strains as well as the effect of stem back extracts of Curtisia dentata on verotoxin production by the verotoxic strains was also investigated. Out of the 69 isolates of E. coli (including O26:H11, O55, O111:NM, 72 O126, O44, O124, O96:H9, O103:H2, O145:NM and O145:H2.) and 41 isolates of Acinetobacter spp. with 26 (53.06%) of the E. coli and 6 (14.63%) of the A. haemolyticus isolates producing verotoxins, and no A. lwoffii isolate produced the toxins. Twenty five - 25(35.23%), 14(20.30%) and 28(40.58%) of the E. coli isolates were positive for VTx1&2, Vtx1 and Vtx2 respectively, 49(71.015%), were positive for extended-spectrum beta-lactamases (ESBLs), 7(77.78%) for serum resistance, 57(82.61%) for cell surface hydrophobicity, 48(69.57%) for gelatinase production and 37(53.62%) for haemolysin production. While transformation occurred among the E. coli and Acinetobacter isolates (transformation frequency: 13.3 x 10-7- 53.4-7), there was poor curing of the plasmid genes, a confirmation of presence of stable antibiotic resistant genes (DNA concentration between 42.7-123.8 μg) and intra-genetic transfer of multidrug resistant genes among isolates. Oxidative stress due to chemicals, salts, alcohol or freeze-thawing (blow temperature stress) exerted various degrees of lethality on E. coli isolates with some bacterial strains losing their potential to express virulence factors with time. There was however, generally insignificant (t test; P≤0.05) lethal effect against all the A. haemolyticus isolates, but crystal violet exerted the highest lethal effect on some individual isolates followed by ethanol, bile salt and NaCl. Isolates from wastewater demonstrated the highest rate of resistance compared to isolates from river water. The cell kill index (CKI) increased as temperature stress (-5; -18; and -28ºC) increased with time. But the rate of loss of expression of virulence factors or viability was slower in isolates from wastewater and abattoir compared to those from river water. Sixty percent of the E. coli isolates showed various levels of resistance to different antibiotics (ampicillin (10 μg), cefuroxime, cephalexin, ceftazidime and tetracycline (30 95 μg in each case)) (multidrug resistance index (MDRI) values 4.20-5.60%). Relative inhibition zone diameters (RIZD) of C. dentata extracts against E. coli serotypes ranged between 8-28% (MIC, 100-2500 μg/ml), while against A. lwoffii and A. haemolyiticus, the RIZD values ranged between 10-28% (MIC, 100-850 μg/ml) and 6-28% (MIC 150-2500 μg/ml) respectively. However, higher MICs (MIC, 70-2500 mg/ml) were recorded for isolates with high MDRI values. Extracts demonstrated inhibitory action against the expression of both Vtx1 and Vtx2 genes in E. coli, A. haemolyticus and A. lwoffii. Saponins, tannins, glycosides, anthraquinones, flavonoids, steroids, phenols quinones, anthocyanins, amines and carboxylic acids were present in C. dentata. Ethanol root bark extracts consistently showed the highest DPPH radical scavenging activity (62.43%), total phenol content (TPH) (57.62 26 mg GAE/g) and reducing power (RP) (41.32%), followed by those of the stem bark and leaf extracts with the respective values of 54.68%, 37.77 mg GAE/g and 21.83%. The extracts also induced the leakage of Na+ and K+ 107 ions from both test bacteria. Detection of virulence factors, antibiotic resistance genes and transformation among these isolates is a very significant outcome that will influence approaches to proactive preventive and control measures and future investigations. Resistant verotoxic A. haemolyticus could further complicate treatment in verotoxic food-borne or nosocomial infections. Induction of cationic leakage by extracts of C. dentata is an indication of one of its mechanism of action on bacterial cells. The plant can therefore be a good source of antibiotic substances for composition as antioxidants or antimicrobials with novel mechanism of action for the treatment of verotoxic bacterial infections.

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20

Johansson, David. "Bacterial toxins for cancer treatment." Doctoral thesis, Umeå universitet, Medicinsk biovetenskap, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1637.

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Even though anti‐cancer chemotherapy has been continuously improved during the last decades. problems with adverse effects and drug resistance still constitutes a considerable obstacle and sets a demand for new effective treatment options. Tissue homeostasis in multi‐cellular organisms is maintained through intrinsic cell death, apoptosis, which removes unwanted or damaged cells. Disrupted apoptosis is an important factor in tumorgenesis and drug resistance, therefore induction or restoration of apoptotic pathways is also important for the treatment of cancer. Several naturally occurring bacterial toxins have the ability to induce apoptosis and could thus be candidates to complement or improve the therapeutic effect of other anticancer drugs. The bacterial toxins, adenylate cyclase (AC) toxin from Bordetella pertussis, α‐toxin from Staphylococcus aureus and verotoxin‐1 (VT‐1) from Escherichia coli were investigated for their ability to induce apoptosis in different tumor cell lines. Toxin induction of cell death was investigated by cell viability assays, end‐stage apoptosis induction by DNA‐fregmentation (TUNEL) assay. Toxin receptor expression and signal transduction pathways to apoptosis were investigated by flow cytometry, caspase enzyme activity assays and western blot. Immunohistochemistry was used for identification of toxin receptor expression in tumor tissue samples. AC‐toxin was cytotoxic and induced apoptosis in cultured malignant plural mesothelioma (MPM) and small‐cell lung cancer (SCLC) cells. Low‐toxic concentrations of AC‐toxin enhanced cisplatin cytotoxicity and apoptosis in both cell lines. MPM‐cells with acquired cisplatin resistance were more sensitive to α‐toxin than the less resistant parental MPM cell line. A low‐toxic concentration of α‐toxin re‐sensitized resistant MPM cells to cisplatin cytotoxicity by apoptosis induced through the mitochondrial pathway without detectable activation of common up‐stream apoptosis signalling proteins. VT‐1 was highly cytotoxic and induced apoptosis in globotriosylceramide (Gb3) ‐expressing glioma, breast cancer and non‐small‐cell lung cancer (NSCLC) cells but was not cytotoxic to non‐Gb3‐expressing cells. PPMP, an inhibitor of glucosylceramide synthesis which makes exposed cells unable to synthesize Gb3 rendered Gb3‐expressing cells resistant to VT‐1. MPM cells with acquired‐cisplatin resistance expressed Gb3 in contrast to the absent of expression in the less resistant parental cell line. Gb3, could however be up‐regulated by cisplatin in Gb3‐negative MPM‐cells. Presence of a low‐toxic concentration of VT‐1 potentiated cisplatin‐induced cytotoxicity and apoptosis in the cisplatin‐resistance MPM cell line. VT‐1 was a potent inducer of apoptosis, probably via stress‐induced Mitogen‐activated protein kinase (MAPK)‐signaling involving c‐Jun N‐terminal kinase (JNK) and p38, leading to disruption of the mitochondrial membrane integrety, activation of caspase‐9 and ‐3, and ultimately DNA fragmentation and cell death. Gb3 expression was demonstrated in clinical specimens of glioblastoma and breast cancer making these tumor types interesting for further VT‐1 studies. We conclude that bacterial toxins may be used to induce apoptosis in several types of cancer cells. Low concentrations of verotoxin‐1 and α‐toxin may potentially be used to overcome acquired cisplatin‐resistance in cancer patients.

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21

Keuerleber, Nina. "Nachweis von Escherichia coli O157 und Shigatoxinen in Rindfleischproben aus dem Landkreis Karlsruhe und Landkreis Rhein- Neckar-Kreis unter Einsatz des Singlepath® E. coli O157 und des Duopath® Verotoxins der Fa. Merck, Darmstadt." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-106232.

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22

Debernardi, Justine. "Le récepteur Gb3/CD77 : analyse de l’apoptose induite par la vérotoxine-1 dans les cellules de lymphome de Burkitt et recherche de ligands endogènes." Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS254.

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Le glycolipide Gb3/CD77 qui est fortement exprimé en surface des cellules de lymphome de Burkitt (LB) est le récepteur d’une toxine bactérienne la Vérotoxine-1 (VT-1). Notre équipe a montré précédemment que, dans les cellules de LB, la VT-1 induit une cascade apoptotique mettant en jeu les caspases et la mitochondrie. Mon travail a consisté à poursuivre l’analyse des bases moléculaires de ce processus, notamment en m’intéressant au rôle de la protéine pro-apoptotique Bid. Bid est un membre de la famille Bcl-2 qui est clivé par la caspase-8 au cours de l’apoptose et dont la forme tronquée (t-Bid) se relocalise à la mitochondrie. Grâce à l’utilisation de clones cellulaires de LB où Bid a été inhibée puis réexprimée sous forme non clivable et d’un inhibiteur de la caspase-8, nous avons montré que lors de l’apoptose induite par la VT1 : 1) la protéine entière Bid (full-length Bid ou FL-Bid) contrôle l’activation de protéines pro-apoptotiques Bax et de Bak ; 2) t-Bid et FL-Bid sont, toutes les deux, impliquées dans la libération des protéines pro-apoptotiques (cytochrome c et Smac/DIABLO) de l’espace intermembranaire de la mitochondrie vers le cytosol ; 3) FL-Bid contrôle l’homodimérisation de Bax et de Bak qui contribuerait à la libération initiale du cytochrome c et de Smac/DIABLO alors que t-Bid est nécessaire à l’hétérodimérisation de Bax et Bak qui permettrait l’amplification de cette libération. L’ensemble de ces résultats montre donc une coopération fonctionnelle entre Bax et Bak au cours de l’apoptose induite par la VT-1 et surtout met en évidence que l’activation de la voie caspase-8/t-Bid n’est absolument pas requise pour initier la mort cellulaire.Gb3/CD77 est aussi exprimé à la surface de certains lymphocytes B normaux, où il constitue un marqueur de différenciation mais sa fonction endogène reste encore indéterminée. Une deuxième partie de mon travail a consisté à essayer d’identifier le ligand physiologique de Gb3/CD77 pour comprendre son rôle biologique. Grâce à une analyse en spectrométrie de masse, nous avons identifié deux protéines potentiellement partenaires de Gb3/CD77 : la galectine-7 et la protéine S100A11
The Gb3/CD77 glycolipid, which is strongly expressed in Burkitt's lymphoma (BL) cells, is a receptor for the bacterial toxin Verotoxin-1 (VT-1). Previously, our group has shown that VT-1 induces an apoptotic pathway in BL cells which is dependent on caspases and mitochondria. Here, we provide new insights into this pathway. A pro-apoptotic member in the Bcl-2 family, Bid is cleaved by caspase-8 and its truncated form t-Bid is translocated to mitochondria. Using LB cell clones where Bid was inhibited prior to being reexpressed as a non-cleavable mutated form (BID D59A) and a caspase-8 inhibitor to explore VT-1-induced apoptosis, we showed that 1) the full length Bid (FL-Bid) controls the activation of pro-apoptotic proteins Bax and Bak; 2) Both t-Bid and FL-Bid are involved in the release of pro-apoptotic proteins (cytochrome c and Smac/DIABLO) from the mitochondrial intermembrane space to the cytosol; 3) FL-Bid controls the homo-oligomerization of both Bax and Bak, likely contributing to the initial release of cytochrome c and Smac/DIABLO while t-Bid is needed for their hetero-oligomerization followed by amplification of the release. Together, these results reveal a functional cooperation between Bax and Bak during VT-1-induced apoptosis and, most importantly, that activation of caspase-8 and t-Bid is not required to induce the onset of cell death. Gb3/CD77 is also expressed in a proportion of normal B-lymphocytes where it constitutes a differentiation marker but whose function remains uncharacterized. In an effort to look for physiological ligands, we have used a biochemical approach followed by mass spectrometry analysis. Two proteins have been identified as potentially Gb3/CD77 partners, namely galectin-7 and protein S100A11

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23

Khan, Mukarram Ahmed. "Global and selective translational effects of verotoxin on the vascular endothelium." 2007. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=789020&T=F.

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Ming-Che, Liu, and 劉明哲. "The antigenic analysis and toxin neutralization test of enterohemorrhagic E.coli verotoxin." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/99365728796785320684.

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碩士
國立屏東科技大學
生物科技研究所
94
Verotoxin（VT）is a major virulent factor of enterohemorrhagic E.coli（EHEC）leading to diarrhea and hemolytic uremic syndrome（HUS）in human. It can also cause diarrhea in animals and even death in some serious cases. VT is classified as VT-I and VT-II base on amino acid sequences. All VT-I and VT-II contain subunit A and B which have 55-57% homology in their amino acid sequences. The B subunit of VT-I binds to its host receptor and then this complex is engulfed by endocytosis leading to death of the cells. The purpose of this study is to identify the antigenic regions of subunit B of VT for development of subunit vaccines. The amino acid sequences with high antigenicity were predicted and amplified by PCR. The correct amplicons were cloned into pET32a vectors, transformed into competent cells, and expressed after induction with IPTG. BALB/c mouse were immunized with the expressed proteins purified with HiTrap affinity columns. Sera from immunized mice were used to probe the recombinant proteins in Western blots. However, results indicated sera reacted with all expressed proteins even negative controls. This suggested these antibodies were induced by fusion tags in pET32a vectors were used for expression of subunit B of VT. Results indicated sera from immunized mice specifically reacted with recombinant proteins. Therefore, epitopes of B subunit of VT were included in the recombinant proteins. Exotoxins of EHEC extracted by polymyxin B were added into Vero cells to calculate 50% cytotoxic dose based on cytopathic effects（CPE）. All sera from immunized mice were mixed with dosages of four CD50 of exotoxins to understand their neutralization titers. Results showed sera raised against VT-I-2, VT-II-1, and VT-II-2 proteins exhibited strong neutralization capabilities with titers up to 80 folds. These results offered useful information for further development of subunit vaccines.

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Shi, Peilin. "Investigating the Anti-viral Property of Verotoxin and its Receptor Gb3 in Preventing Primary HIV-1 Infection." Thesis, 2011. http://hdl.handle.net/1807/31440.

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Verotoxin produced by Enterohemorrhagic E. coli is comprised of a catalytic A subunit and a receptor Gb3 binding B subunit pentamer. VT causes protein synthesis inhibition by ribosomal inactivation in Gb3 positive cells via receptor mediated endocytosis and retrograde transport to the ER. We propose that verotoxin is a novel inhibitor for HIV-1 infection. Experiments conducted using VT treated Jurkat-C T cells and PHA/IL-2 activated human PBMCs reveal the anti-HIV-1 property of VT is receptor Gb3 independent since the catalytic A subunit alone is sufficient for inhibition. Possible mechanism of action involves mild inhibition of protein synthesis and cell proliferation. Recent findings in our lab suggest Gb3 is a natural resistance factor for HIV-1 infection, which was further investigated by selecting a Gb3 low subpopulation in THP-1 cells using VT treatment. Selected THP-1 cells were completely resistant to HIV-1 infection, however decreased surface CXCR4 expression may be a cause.

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26

Schillberg, Erin. "Risk factors associated with sporadic Campylobacter, Salmonella and verotoxin-producing Escherichia coli in different regions within Manitoba." 2009. http://hdl.handle.net/1993/29784.

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Schwenk, Petra. "Quantitativer und qualitativer Nachweis Verotoxin-bildender E. coli-Stämme (VTEC) in Kotproben und auf Tierkörpern geschlachteter Schafe mit Hilfe PCR-amplifizierter Gensonden /." 2000. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=009223533&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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28

Schotte, Ulrich [Verfasser]. "Bewertung des Infektionsrisikos für den Verpflegungsteilnehmer der Bundeswehr durch Verotoxin-bildende Escherichia coli (VTEC) unter besonderer Berücksichtigung streichfähiger und schnittfester Rohwürste / eingereicht von Ulrich Schotte." 2003. http://d-nb.info/967351294/34.

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29

Keuerleber, Nina [Verfasser]. "Nachweis von Escherichia coli O157 und Shigatoxinen in Rindfleischproben aus dem Landkreis Karlsruhe und Landkreis Rhein-Neckar-Kreis unter Einsatz des Singlepath E. coli O157 und des Duopath Verotoxins der Fa. Merck, Darmstadt / von Nina Anabel Keuerleber." 2009. http://d-nb.info/997592796/34.

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Dissertations / Theses on the topic 'Verotoxine'

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