Journal articles: 'Verotoxine'

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Dobrescu, Lucia, and L. Renault. "Recherche de la neurotoxine (verotoxine) à partir de souches d ’Escherichia coli isolées de diarrhée colibacillaire du porcelet sevré." Bulletin de l'Académie Vétérinaire de France, no. 2 (1989): 199. http://dx.doi.org/10.4267/2042/64632.

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Bradley, D. E., S. P. Howard, and H. Lior. "Colicinogeny of O157:H7 enterohemorrhagic Escherichia coli and the shielding of colicin and phage receptors by their O-antigenic side chains." Canadian Journal of Microbiology 37, no. 2 (February 1, 1991): 97–104. http://dx.doi.org/10.1139/m91-014.

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Twenty O157:H7 enterohemorrhagic Escherichia coli strains from patients with different clinical conditions were tested for colicinogeny and the presence of Verotoxin (VT) genes. From bloody diarrhea cases, 7/8 isolates and from hemolytic uremic syndrome cases 3/5 isolates all synthesized what appeared to be colicin D. The remaining strains, which included 7 from asymptomatic sources, were noncolicinogenic. The plasmid determining the colicin was found to be 1.4 kb larger than the 5.2-kb pColD. The colicin D protein had a molecular weight of about 90 000, whereas the O157 colicin was 87 000. The plasmid was designated pColD157 to reflect these differences. Of O157:H7 isolates 17/20 had genes for both of the Verotoxins VT1 and VT2, and the remaining 3/20 for VT1 only. There was no correlation between the presence of VT determinants and colicinogeny or symptoms. The O157:H7 strains exhibited significant resistance to other colicins and bacteriophages. Key words: O-antigens, enterohemorrhagic, colicin, Verotoxin, bacteriophages.

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BASKARAN, SANGEETHA ANANDA, ANUP KOLLANOOR-JOHNY, MEERA SURENDRAN NAIR, and KUMAR VENKITANARAYANAN. "Efficacy of Plant-Derived Antimicrobials in Controlling Enterohemorrhagic Escherichia coli Virulence In Vitro." Journal of Food Protection 79, no. 11 (November 1, 2016): 1965–70. http://dx.doi.org/10.4315/0362-028x.jfp-16-104.

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ABSTRACTEscherichia coli O157:H7 is a major foodborne pathogen that can cause serious human illness characterized by hemorrhagic diarrhea and kidney failure. The pathology of enterohemorrhagic E. coli O157:H7 (EHEC) infection is primarily mediated by verotoxins, which bind to the globotriaosylceramide receptor on host cells. Antibiotics are contraindicated for treating EHEC infection because they lead to increased verotoxin release, thereby increasing the risk of renal failure and death in patients. Thus, alternative strategies are needed for controlling EHEC infections in humans. This study investigated the effect of subinhibitory concentrations of five plant-derived antimicrobial agents (PDAs) that are generally considered as safe, i.e., trans-cinnamaldehyde, eugenol, carvacrol, thymol, and β-resorcylic acid, on EHEC motility, adhesion to human intestinal epithelial cells, verotoxin production, and virulence gene expression. All tested PDAs reduced EHEC motility and attachment to human intestinal epithelial cells (P < 0.05) and decreased verotoxin synthesis by EHEC. The reverse transcription real-time PCR data revealed that PDAs decreased the expression of critical virulence genes in EHEC (P < 0.05). The results collectively suggest that these PDAs could be used to reduce EHEC virulence, but follow-up studies in animal models are necessary to validate these findings.

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Khan, Md Fazlul Karim, and Shah Samiur Rashid. "Molecular Characterization of Plasmid-Mediated Non-O157 Verotoxigenic Escherichia coli Isolated from Infants and Children with Diarrhea." Baghdad Science Journal 17, no. 3 (September 1, 2020): 0710. http://dx.doi.org/10.21123/bsj.2020.17.3.0710.

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A significant increase in the incidence of non-O157 verotoxigenic Escherichia coli (VTEC) infections have become a serious health issues, and this situation is worsening due to the dissemination of plasmid mediated multidrug-resistant microorganisms worldwide. This study aims to investigate the presence of plasmid-mediated verotoxin gene in non-O157 E. coli. Standard microbiological techniques identified a total of 137 E. coli isolates. The plasmid was detected by Perfectprep Plasmid Mini preparation kit. These isolates were subjected to disk diffusion assay, and plasmid curing with ethidium bromide treatment. The plasmid containing isolates were subjected to a polymerase chain reaction (PCR) for investigating the presence of plasmid mediated verotoxin gene (VT1 and VT2) in non-O157 E. coli. Among the 137 E. coli isolates, 49 isolates were non-O157 E. coli while 29 (59.1%) isolates were verotoxin producing non-O157 serotypes and 26 non-O157 VTEC isolates possessed plasmids. Certain isolates harboured single sized plasmid while others had multiple plasmids with different size varied from 1.8kb to 7.6kb. A plasmid containing all (100%) the isolates was multidrug-resistant. Eight isolates changed their susceptibility patterns while three isolates were found to lose plasmid after post plasmid curing treatment and the rest of the isolates (15) remained constant. Different PCR sets characterized 3 plasmid-mediated verotoxins producing non-O157 E. coli. This current study demonstrated the occurrence of plasmid mediated verotoxin gene in non-O157 E. coli. To the best of our knowledge, this is the first report in the global literature on plasmid-mediated verotoxin gene in non-O157 E. coli. Timely diagnosis and surveillance of VTEC infections should prioritize to stop or slow down the virulence gene for dissemination by plasmid-mediated gene transfer amongst the same bacteria or other species.

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Mackenzie, A. M. R., P. Lebel, E. Orrbine, P. C. Rowe, L. Hyde, F. Chan, W. Johnson, and P. N. McLaine. "Sensitivities and Specificities of Premier E. coliO157 and Premier EHEC Enzyme Immunoassays for Diagnosis of Infection with Verotoxin (Shiga-Like Toxin)-Producing Escherichia coli." Journal of Clinical Microbiology 36, no. 6 (1998): 1608–11. http://dx.doi.org/10.1128/jcm.36.6.1608-1611.1998.

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This study describes the performance of two rapid enzyme immunoassays, Premier E. coli O157 and Premier EHEC (Meridian Diagnostics Inc., Cincinnati, Ohio) for the detection in stools of Escherichia coli O157 and verotoxins (Shiga-like toxins), respectively. Both tests were performed on stools from 876 children presenting to eight emergency departments with diarrhea. Standard culture, including E. coli O157:H7 isolation, was performed, and paired sera were taken for anti-O157-lipopolysaccharide antibody determination. Stools from patients enrolled in the study, and those yielding discordant results, were sent to a reference laboratory for repeat testing and further investigation, including cytotoxicity and non-O157 verotoxin-producingE. coli culture. Results were classified as field results (obtained in the eight site laboratories) and resolved results (obtained after repeat testing in the central laboratory). The “gold standard” for sensitivity of both tests and for specificity of Premier E. coli O157 was isolation of E. coli O157:H7 or a fourfold anti-O157 antibody rise. Specimens positive by the Premier EHEC test and negative for E. coli O157 culture were examined for non-O157 verotoxin-producingE. coli. The field sensitivity of PremierE. coli O157 was 86%, that of Premier EHEC was 89%, and the specificity of Premier E. coli O157 was 98%. Ten of 13 discordant Premier E. coli O157 results were reassigned as true results after repeat testing. Ten non-O157 verotoxin-producing E. coli isolates were recovered from Premier EHEC-positive, E. coli O157 culture-negative stools. Only one specimen gave an unequivocally false-positive Premier EHEC result. Both tests are highly sensitive and are specific if correctly performed. The Premier EHEC test will be particularly valuable as a practical routine test for the detection of non-O157 verotoxin-producing E. coli.

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Leung, P. H. M., J. S. M. Peiris, W. W. S. Ng, and W. C. Yam. "Polyclonal Antibodies to Glutathione S-Transferase- Verotoxin Subunit A Fusion Proteins Neutralize Verotoxins." Clinical and Vaccine Immunology 9, no. 3 (May 2002): 687–92. http://dx.doi.org/10.1128/cdli.9.3.687-692.2002.

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ABSTRACT The A1 subunits of verotoxin-1 (VT1) and VT2 genes were cloned into pGEX-4T-2 for the expression of glutathione S-transferase (GST) fusion proteins. The N-terminal and the transmembrane regions of the A1 subunits were excluded from the constructs in order to increase the product yields. Polyclonal anti-VT1A1 and anti-VT2A1 antibodies were produced by immunizing rabbits with GST-VT1A1 and GST-VT2A1 fusion proteins, respectively. The antibodies were tested for their ability to neutralize active toxins from 45 VT-producing Escherichia coli (VTEC) strains. The antibodies had significantly high neutralizing activities against their homologous toxins. The average percentages of neutralization of VT1 by anti-GST-VT1A1 and anti-GST-VT2A1 were 76.7% ± 7.9% and 3.6% ± 2.3%, respectively, and those of VT2 were 1.7% ± 2.3% and 82.5% ± 13.9%, respectively. VT2 variant toxin was neutralized by anti-GST-VT2A1, with cross neutralization being a possible consequence of sequence homology between VT2 and a VT2 variant. To our knowledge, this is the first report on the production of polyclonal antibodies from GST-VT fusion proteins. The antibodies were shown to exhibit specific toxin neutralizing activities and may be useful for immunological diagnosis of VTEC infections.

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Krüger, Alejandra, Paula M. A. Lucchesi, and Alberto E. Parma. "Verotoxins in Bovine and Meat Verotoxin-ProducingEscherichia coliIsolates: Type, Number of Variants, and Relationship to Cytotoxicity." Applied and Environmental Microbiology 77, no. 1 (October 29, 2010): 73–79. http://dx.doi.org/10.1128/aem.01445-10.

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ABSTRACTIn this study, we determinedvtsubtypes and evaluated verotoxicity in basal as well as induced conditions of verotoxin-producingEscherichia coli(VTEC) strains isolated from cattle and meat products. Most (87%) of the 186 isolates carried avt2gene. Moreover, thevt2subtype, which is associated with serious disease, was present in 42% of our VTEC collection. The othervtsubtypes detected werevt1,vt1d,vt2vha,vt2vhb,vt2O118,vt2d(mucus activatable), andvt2g. A total of 41 (22%) of the isolates possessed more than onevtsubtype in its genome, and among them the most frequent combination wasvt1/vt2, but we also observed multiple combinations amongvt2subtypes. Differences in verotoxicity titers were found among a selection of 54 isolates. Among isolates with a singlevt2variant, those carrying thevt2subtype had high titers under both uninduced and induced conditions. However, the highest increase in cytotoxicity under mitomycin C treatment was detected among the strains carryingvt2vhaorvt2hbvariants. Notably, the isolates carrying thevt1subtype showed a lesser increase than that of most of thevt2-positive VTEC strains. Furthermore, the presence of more than onevtgene variant in the same isolate was not reflected in higher titers, and generally the titers were lower than those for strains with only one gene variant. The main observation was that both basal and induced cytotoxic effects seemed to be associated with the type and number ofvtvariants more than with the serotype or origin of the isolate.

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Maloney, M. D., and C. A. Lingwood. "CD19 has a potential CD77 (globotriaosyl ceramide)-binding site with sequence similarity to verotoxin B-subunits: implications of molecular mimicry for B cell adhesion and enterohemorrhagic Escherichia coli pathogenesis." Journal of Experimental Medicine 180, no. 1 (July 1, 1994): 191–201. http://dx.doi.org/10.1084/jem.180.1.191.

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The glycosphingolipid globotriaosyl ceramide (CD77) and other globo-series glycolipids containing terminal galactose (Gal)alpha 1-4Gal residues function as receptors for the verotoxin (Shiga-like toxin) family of Escherichia coli-elaborated toxins. CD77 is also a marker for germinal center B lymphocytes and Burkitt's lymphoma cells. The pan B cell marker CD19 is a 95-kD membrane protein that appears early in B cell differentiation and is only lost upon terminal differentiation to plasma cells. CD19 is involved in signal transduction and has a regulatory role in B cell proliferation and differentiation in response to activation in vitro. However, an endogenous ligand for CD19 has not yet been identified. We report herein that the extracellular domain of CD19 has a potential CD77-binding site with extensive sequence similarity to the verotoxin B-subunits. These B-subunit-like sequences on CD19 are in close proximity following the organization of intervening amino acids into disulfide-linked domains. Cocapping of CD19 and CD77 on Burkitt's lymphoma-derived Daudi cells with anti-CD19 antibodies indicates that CD19 and CD77 are associated on the B cell surface. Cell surface binding of anti-CD19 antibodies is decreased on CD77-deficient mutant Daudi cells, suggesting that CD77 expression influences the surface expression of CD19. Wild-type Daudi cells, but not the CD19/CD77-deficient mutants, bind to matrices expressing the carbohydrate moiety of CD77 or other Gal alpha 1-4Gal containing glycolipids. This binding can be inhibited by anti-CD77 antibodies, the CD77-binding verotoxin B-subunit or anti-CD19 antibodies. Daudi cells exhibit a degree of spontaneous homotypic adhesion in culture while the CD77/CD19-deficient Daudi mutants grow as single cells. The stronger homotypic adhesion that occurs in B cells after antibody ligation of CD19 and that involves, to some extent, the integrin system, is also dramatically lower in the mutant cells relative to the parent cell line. However, reconstitution of mutant cells with CD77 restores the anti-CD19 mAb-induced adhesion to wild-type Daudi cell levels. These studies represent the first time that CD19-mediated signaling has been reconstituted in a low-responder B cell line. These convergent observations provide compelling evidence that CD19/CD77 interactions function in adhesion and signal transduction at a specific stage in B cell development and suggest that such interactions have a role in B lymphocyte homing and germinal center formation in vivo. By targeting CD77+ B cells, verotoxins may suppress the humoral arm of the immune response during infection.(ABSTRACT TRUNCATED AT 400 WORDS)

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Yuk, Hyun-Gyun, and Douglas L. Marshall. "Heat Adaptation Alters Escherichia coli O157:H7 Membrane Lipid Composition and Verotoxin Production." Applied and Environmental Microbiology 69, no. 9 (September 2003): 5115–19. http://dx.doi.org/10.1128/aem.69.9.5115-5119.2003.

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ABSTRACT The influence of heat adaptation (growth at 42 and 45°C) on changes in membrane lipid composition and verotoxin concentration of Escherichia coli O157:H7 (ATCC 43895), an rpoS mutant of ATCC 43895 (FRIK 816-3), a verotoxin mutant E. coli O157:H7 (B6-914), and nonpathogenic E. coli (ATCC 25922) was investigated. D values (57°C) of heat-adapted cells were up to 3.9 min longer than those of control cells for all four strains. Heat adaptation increased the amounts of palmitic acid (16:0) and cis-vaccenic acid (18:1ω7c) in membrane lipids of ATCC 43895 and the rpoS mutant, whereas there was a reduction and no change in the amount of cis-vaccenic acid in nonpathogenic and verotoxin mutant E. coli, respectively. The ratio of palmitic to cis-vaccenic acids decreased in ATCC 43895 and in the rpoS mutant, whereas the ratio increased in nonpathogenic E. coli and was not different in the verotoxin mutant with elevated growth temperature. Total verotoxin concentration decreased due to a reduction in intracellular verotoxin amount in heat-adapted ATCC 43895 and rpoS mutant strains. However, extracellular verotoxin concentration increased in heat-adapted cells. The rpoS gene did not influence membrane lipid composition changes although it did affect heat resistance. Results suggest that increased membrane fluidity may have caused increased verotoxin secretion.

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Dove, Alan. "Anticancer verotoxin." Nature Biotechnology 17, no. 8 (August 1999): 738. http://dx.doi.org/10.1038/11646.

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Jores, Joerg, Karen Zehmke, Juergen Eichberg, Leonid Rumer, and Lothar H. Wieler. "Description of a Novel Intimin Variant (Type ζ) in the Bovine O84:NM Verotoxin-Producing Escherichia coli Strain 537/89 and the Diagnostic Value of Intimin Typing." Experimental Biology and Medicine 228, no. 4 (April 2003): 370–76. http://dx.doi.org/10.1177/153537020322800407.

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Infections with verotoxin-producing Escherichia coli (VTEC) has resulted in increasing numbers of human illnesses annually. These illnesses usually result from the ability of VTEC to cause the attaching and effacing lesions (AE lesion). The AE phenotype is encoded by the locus of enterocyte effacement (LEE) pathogenicity island. A key adhesion factor involved is the outer membrane protein intimin, encoded by the eae gene within the LEE. Intimin types α, β, γ, δ, and ε have been described previously. Each intimin represents distinct phylogenetic lineages of LEE-positive strains. A new intimin type ζ was identified in a VTEC strain of the serotype O84:NM (nonmotile) that was isolated from a calf with diarrhea. ζ intimin showed the highest similarity (88%) of its amino acid sequence to the α intimin. For diagnostic purposes, we established a polymerase chain reaction (PCR) method for diagnosis of the key virulence traits of VTEC (i.e., verotoxins and intimins). This method also distinguishes between the toxins (VT1 and VT2) and the six intimin types. By applying the PCR method, intimin ζ in strains of other VTEC serotypes O84:H2, O92:NM, O119:H25, and O150:NM was identified. Because the intimin types represent distinctive phylogenetic E. coli lineages, application of the intimin subtyping PCR offers significant benefits. These include improving diagnosis of VTEC infection and increasing the understanding of evolution of attaching and effacing VTEC and other LEE-positive bacteria.

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Lingwood, C. A., A. A. Khine, and S. Arab. "Globotriaosyl ceramide (Gb3) expression in human tumour cells: intracellular trafficking defines a new retrograde transport pathway from the cell surface to the nucleus, which correlates with sensitivity to verotoxin." Acta Biochimica Polonica 45, no. 2 (June 30, 1998): 351–59. http://dx.doi.org/10.18388/abp.1998_4230.

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The verotoxin receptor globotriaosyl ceramide (Gb3) is overexpressed in an ovarian tumour resistant to chemotherapy. An overlay of frozen tumour sections shows extensive staining of the tumour cells with verotoxin B subunit. In addition, blood vessels within the tumour mass are stained. The sensitivity of ovarian tumour cells in vitro to verotoxin can be modulated by culturing the cells in sodium butyrate to obtain an approximately 5000-fold increase in susceptibility. This increased susceptibility is correlated with the intracellular targeting of verotoxin as monitored by using FITC-VT B subunit, in that prior to sodium butyrate treatment the toxin is internalized to a juxtanuclear (likely) Golgi location whereas, following butyrate treatment the intracellular toxin is distributed around the nucleus, consistent with endoplasmic reticulum and nuclear envelope location. This perinuclear location is similar to that found for drug-resistant variants of ovarian tumour cell lines. These results suggest that intracellular targeting of verotoxin to the perinuclear area results in increased cytotoxicity. Potentially such targeting may also occur in other human tumours.

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Adamatzky, Andrew. "Computing in Verotoxin." ChemPhysChem 18, no. 13 (June 13, 2017): 1822–30. http://dx.doi.org/10.1002/cphc.201700477.

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Cooling, Laura L. W., Katherine E. Walker, Theresa Gille, and Theodore A. W. Koerner. "Shiga Toxin Binds Human Platelets via Globotriaosylceramide (Pk Antigen) and a Novel Platelet Glycosphingolipid." Infection and Immunity 66, no. 9 (September 1, 1998): 4355–66. http://dx.doi.org/10.1128/iai.66.9.4355-4366.1998.

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ABSTRACT Hemolytic-uremic syndrome is a clinical syndrome characterized by acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia that often follows infection by Shiga toxin- or verotoxin-producing strains of Escherichia coli. Because thrombocytopenia and platelet activation are hallmark features of hemolytic-uremic syndrome, we examined the ability of Shiga toxin to bind platelets by flow cytometry and high-performance thin-layer chromatography (HPTLC) of isolated platelet glycosphingolipids. By HPTLC, Shiga toxin was shown to bind globotriaosylceramide (Gb3) and a minor platelet glycolipid with anRf of 0.03, band 0.03. In a survey of 20 human tissues, band 0.03 was identified only in platelets. In individuals, band 0.03 was expressed by 20% of donors and was specifically associated with increased platelet Gb3 expression. Based on glycosidase digestion and epitope mapping, band 0.03 was hypothesized to represent a novel glycosphingolipid, IV3-β-Galα1-4galactosylglobotetraosylceramide. Based on incidence, structure, and association with increased Gb3 expression, band 0.03 may represent the antithetical Luke blood group antigen. By flow cytometry, Shiga toxin bound human platelets, although the amount of Shiga toxin bound varied in donors. Differences in Shiga toxin binding to platelet membranes did not reflect differences in platelet Gb3 expression. In contrast, there was a loose association between Shiga toxin binding and decreasing forward scatter, suggesting that Shiga toxin and verotoxins bind more efficiently to smaller, older platelets. In summary, Shiga and Shiga-like toxins may bind platelets via specific glycosphingolipid receptors. Such binding may contribute to the thrombocytopenia, platelet activation, and microthrombus formation observed in hemolytic-uremic syndrome.

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Karama, Musafiri, Roger P. Johnson, Robert Holtslander, and Carlton L. Gyles. "Production of Verotoxin and Distribution of O Islands 122 and 43/48 among Verotoxin-Producing Escherichia coli O103:H2 Isolates from Cattle and Humans." Applied and Environmental Microbiology 75, no. 1 (November 7, 2008): 268–70. http://dx.doi.org/10.1128/aem.01445-08.

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ABSTRACT This study investigated variations in the occurrence of markers of O islands 122 and 43/48 and in verotoxin 1 production in 91 verotoxin-producing Escherichia coli (VTEC) O103:H2 strains of bovine and human origins. None of the genes that were investigated appear to be virulence indicators for human O103:H2 VTEC.

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Rowe, P. C., E. Orrbine, H. Lior, G. A. Wells, and P. N. McLaine. "A prospective study of exposure to verotoxin-producingEscherichia coliamong Canadian children with haemolytic uraemic syndrome." Epidemiology and Infection 110, no. 1 (February 1993): 1–7. http://dx.doi.org/10.1017/s0950268800050615.

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SUMMARYHaemolytic uraemic syndrome (HUS) is a leading cause of acute renal failure in childhood. Although infection withEscherichia coliO 157. H7 has been associated with HUS in North America and Europe, only a limited number of studies have examined the role of other verotoxin-producingE. coli(VTEC) serotypes in this condition. To address this issue, we conducted a comprehensive, prospective microbiological study of patients treated for HUS at eight Canadian hospitals in the summer of 1990. Of the 34 consecutive patients with HUS enrolled over 4 months,E. coli0 157. H7 was isolated from the stools of 26, and otherE. coliserotypes were isolated from four patients. In four subjects no pathogenicE. coliserotypes were identified on stool culture. Using oligonucleotide probes specific for VT-1 and VT-2, verotoxin genes were detected in the stool isolates of all patients withE. coliO 157.H7, and from two with otherE. coliserotypes. Two other patients had at least a fourfold rise in anti-verotoxin antibodies. Strong evidence of exposure to a verotoxin was present in 30/34 (88%). Patients withE. coli0 157.H7 infection were more likely to develop an antibody response to VT-2 than to VT-1 (22/22 vs 12/22; P = 0.002). These results further strengthen the association of HUS with verotoxin-producingE. coliin North America, and confirm thatE. coliserotypes other than 0 157. H7 are isolated in a small proportion of summertime HUS episodes.

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Philpott, Dana J., Cameron A. Ackerley, Amanda J. Kiliaan, Mohamed A. Karmali, Mary H. Perdue, and Philip M. Sherman. "Translocation of verotoxin-1 across T84 monolayers: mechanism of bacterial toxin penetration of epithelium." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 6 (December 1, 1997): G1349—G1358. http://dx.doi.org/10.1152/ajpgi.1997.273.6.g1349.

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Verotoxin-producing Escherichia coli (VTEC) are pathogenic bacteria associated with diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome. Verotoxins (VTs) elaborated by these organisms produce cytopathic effects on a restricted number of cell types, including endothelial cells lining the microvasculature of the bowel and the kidney. Because human intestinal epithelial cells lack the globotriaosylceramide receptor for VT binding, it is unclear how the toxin moves across the intestinal mucosa to the systemic circulation. The aims of this study were to determine the effects of VT-1 on intestinal epithelial cell function and to characterize VT-1 translocation across monolayers of T84 cells, an intestinal epithelial cell line. VT-1 at concentrations up to 1 μg/ml had no effect on the barrier function of T84 monolayers as assessed by measuring transmonolayer electrical resistance (102 ± 8% of control monolayers). In contrast, both VT-positive and VT-negative VTEC bacterial strains lowered T84 transmonolayer resistance (45 ± 7 and 38 ± 6% of controls, respectively). Comparable amounts of toxin moved across monolayers of T84 cells, exhibiting high-resistance values, as monolayers with VTEC-induced decreases in barrier function, suggesting a transcellular mode of transport. Translocation of VT-1 across T84 monolayers paralleled the movement of a comparably sized protein, horseradish peroxidase. Immunoelectron microscopy confirmed transcellular transport of VT-1, since the toxin was observed within endosomes and associated with specific intracellular targets, including the Golgi network and endoplasmic reticulum. These data present a mode of VT-1 uptake by toxin-insensitive cells and suggest a general mechanism by which bacterial toxins lacking specific intestinal receptors can penetrate the intestinal epithelial barrier.

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YUK, HYUN-GYUN, and DOUGLAS L. MARSHALL. "Influence of Acetic, Citric, and Lactic Acids on Escherichia coli O157:H7 Membrane Lipid Composition, Verotoxin Secretion, and Acid Resistance in Simulated Gastric Fluid†." Journal of Food Protection 68, no. 4 (April 1, 2005): 673–79. http://dx.doi.org/10.4315/0362-028x-68.4.673.

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The effect of organic acid (acetic, citric, and lactic acids) adaptation at equivalent initial pH values (6.4 and 5.4) on changes in membrane lipid composition, verotoxin concentration, and acid resistance in simulated gastric fluid (pH 1.5, 37°C) was determined for Escherichia coli O157:H7 ATCC 43895 (HEC) and an rpoS mutant of E. coli O157:H7 ATCC 43895 (RM, FRIK 816-3). For HEC, lactic acid–adapted (pH 5.4) cells had the greatest D-value (32.2 min) and acetic acid–adapted (pH 5.4) cells had the smallest D-value (16.6 min) in simulated gastric fluid. For RM, D-values of citric and acetic acid–adapted cells were similar to those for nonadapted cells grown at pH 7.3, but D-values increased from 13.1 to 27.9 min in lactic acid–adapted cells (from pH 7.3 to pH 5.4). For both strains, the ratio of cis-vaccenic to palmitic acids decreased for citric and lactic acid–adapted cells, but the ratio increased for acetic acid–adapted cells at pH 5.4. Organic acid–adapted cells produced less total verotoxin than did nonadapted cells at approximately 108 CFU/ml. Extracellular verotoxin concentration proportionally decreased with decreasing pH for both HEC and RM. Changes in membrane lipid composition, verotoxin concentration, and acid resistance in HEC and RM were dependent on both pH and organic acid. Deletion of the rpoS gene did not affect these changes but did decrease acid resistance in citric acid–adapted cells. Results indicate that decreased membrane fluidity may have caused increased acid resistance and decreased verotoxin secretion.

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GARBER, L., S. WELLS, L. SCHROEDER-TUCKER, and K. FERRIS. "Factors Associated with Fecal Shedding of Verotoxin-Producing Escherichia coli O157 on Dairy Farms." Journal of Food Protection 62, no. 4 (April 1, 1999): 307–12. http://dx.doi.org/10.4315/0362-028x-62.4.307.

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Fecal samples were collected from 4,361 dairy cows on 91 dairy operations between 26 February and 8 July 1996. Fecal samples were cultured for Escherichia coli O157, and positive isolates were probed for verotoxin-producing genes. A total of 52 (1.2%) fecal samples on 22 (24.2%) operations were positive for verotoxin-producing E. coli O157. Herds in which samples were collected on or after 1 May 1996 were significantly more likely to test positive than herds sampled before that date (odds ratio = 7.7). Herds maintained on farms on which alleyways were flushed with water to remove manure were 8.0 times more likely to have samples test positive for verotoxin-producing E. coli O157 than were herds maintained on farms cleaned by use of other methods of manure removal.

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Lingwood, C. A., S. Arab, A. A. Khine, and P. Tam. "Nuclear targeting of verotoxin." Biochemistry and Cell Biology 77, no. 4 (August 25, 1999): 402. http://dx.doi.org/10.1139/o99-903w.

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PALUMBO, SAMUEL A., ALLAN PICKARD, and JEFFREY E. CALL. "Population Changes and Verotoxin Production of Enterohemorrhagic Escherichia coli Strains Inoculated in Milk and Ground Beef Held at Low Temperatures." Journal of Food Protection 60, no. 7 (July 1, 1997): 746–50. http://dx.doi.org/10.4315/0362-028x-60.7.746.

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This study investigated the influence of low temperature and background flora on growth and verotoxin production by strains of enterohemorrhagic Escherichia coli in milk and ground beef. In the presence of no or low background flora, there was growth of the strains at 8°C. High background flora in ground beef inhibited growth at this temperature. In the foods held at low temperatures, only small amounts of verotoxin were detected; however, even at the optimum 37°C, there was still relatively little verotoxin formed compared to that in broth cultures. Even under nongrowth conditions (high background flora or 5°C holding temperature), the strains remained viable. These data suggest any food contaminated by these bacteria and held at the recommended temperature of 5°C will remain hazardous, and under certain conditions, holding at temperatures :≥8°Cwould increase the hazard.

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Lingwood, C. A., and S. K. Yiu. "Glycolipid modification of α2 interferon binding. Sequence similarity between the α2 interferon receptor and verotoxin (Shiga-like toxin) B-subunit." Biochemical Journal 283, no. 1 (April 1, 1992): 25–26. http://dx.doi.org/10.1042/bj2830025.

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Previous studies have implicated the glycolipid receptor for the Escherichia coli-derived verotoxin, globotriaosylceramide (Gb3; Gal alpha 1-4Gal beta 1-4Glc-ceramide), in the mechanism of alpha 2 interferon signal transduction. Comparison of the amino acid sequence of the human alpha 2 interferon receptor with that of the B (receptor-binding)-subunit of verotoxin shows three regions of similarity which may provide a structural basis for alpha 2-interferon-receptor/Gb3 interaction.

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Yuk, Hyun-Gyun, and Douglas L. Marshall. "Adaptation of Escherichia coli O157:H7 to pH Alters Membrane Lipid Composition, Verotoxin Secretion, and Resistance to Simulated Gastric Fluid Acid." Applied and Environmental Microbiology 70, no. 6 (June 2004): 3500–3505. http://dx.doi.org/10.1128/aem.70.6.3500-3505.2004.

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ABSTRACT The influence of adaptation to pH (from pH 5.0 to 9.0) on membrane lipid composition, verotoxin concentration, and resistance to acidic conditions in simulated gastric fluid (SGF) (pH 1.5, 37Ã¯Â¿Â½C) was determined for Escherichia coli O157:H7 (HEC, ATCC 43895), an rpoS-deficient mutant of ATCC 43895 (HEC-RM, FRIK 816-3), and nonpathogenic E. coli (NPEC, ATCC 25922). Regardless of the strain, D values (in SGF) of acid-adapted cells were higher than those of non-acid-adapted cells, with HEC adapted at pH 5.0 having the greatest D value, i.e., 25.6 min. Acid adaptation increased the amounts of palmitic acid (C16:0) and decreased cis-vaccenic acid (C18:1ω7c) in the membrane lipids of all strains. The ratio of cis-vaccenic acid to palmitic acid increased at acidic pH, causing a decrease in membrane fluidity. HEC adapted to pH 8.3 and HEC-RM adapted to pH 7.3 exhibited the greatest verotoxin concentrations (2,470 and 1,460 ng/ml, respectively) at approximately 108 CFU/ml. In addition, the ratio of extracellular to intracellular verotoxin concentration decreased at acidic pH, possibly due to the decrease of membrane fluidity. These results suggest that while the rpoS gene does not influence acid resistance in acid-adapted cells it does confer decreased membrane fluidity, which may increase acid resistance and decrease verotoxin secretion.

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Devenish, John, Carlton Gyles, and Jonathan LaMarre. "Binding ofEscherichia coliverotoxins to cell surface protein on wild-type and globotriaosylceramide-deficient Vero cells." Canadian Journal of Microbiology 44, no. 1 (January 1, 1998): 28–34. http://dx.doi.org/10.1139/w97-123.

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We have examined verotoxin (VT) binding to cell surface proteins. When Vero or globotriaosylceramide (Gb3) deficient Vero (VRP) cells were incubated with125I-labelled verotoxin 2 (VT2) and disuccinimidyl suberate cross-linker, SDS-PAGE of cell lysates showed radiolabelled bands at 44, 50, 60, 86, 102, and 138 kDa. When125I-labelled verotoxin 1 (VT1) was cross-linked, radioactive bands occurred at 51, 67, 101, 160, 188, and 232 kDa. In contrast,125I-labelled VT1 B subunit produced a single radioactive band migrating at 50 kDa. CHO cells did not bind labelled VT. VT2 binding to VRP cells fit a rectangular hyperbola suggesting a single class of binding sites. In contrast, VT1 and VT1 B subunit binding to VRP cells was best fit by sigmoidal curves suggesting the presence of positive cooperativity between at least two binding sites. Scatchard analysis of VT2 binding data yielded 3.5 times 109molecules bound/ µg of cell protein with an equilibrium dissociation constant (KD) of 13 nM. The apparent KDwas 9.7 nM for VT1 and 73.2 nM for VT1 B subunit. These results indicate that VT binds to a protein, or proteins, on the surface of susceptible cells and that there appear to be differences between VT1 and VT2 binding. Interactions between VT1 or VT2 and the proteins demonstrated here may be important in the biological activity of VT.Key words: verotoxin, protein receptors, hemolytic uremic syndrome, Escherichia coli.

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Thompson, Laura H., Sandra Giercke, Carole Beaudoin, David Woodward, and John L. Wylie. "Enhanced Surveillance of non-O157 Verotoxin-ProducingEscherichia coliin Human Stool Samples from Manitoba." Canadian Journal of Infectious Diseases and Medical Microbiology 16, no. 6 (2005): 329–34. http://dx.doi.org/10.1155/2005/859289.

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BACKGROUND: Relatively few enhanced surveillance studies have been undertaken to investigate the extent to which verotoxin-producing non-O157 serotypes ofEscherichia colioccur in stool samples received for the detection of verotoxin-producing organisms.OBJECTIVES: To describe the prevalence, molecular and epidemiological characteristics, and geographical patterns associated with non-O157 verotoxin-producingE coli(VTEC) in Manitoba.RESULTS: Thirty-two VTEC isolates consisting of 10 serogroups and 13 different serotypes were isolated over a 22-month period. Twenty-three isolates (71.8%) possessed verotoxin-encoding gene stx1 only, five isolates (15.6%) possessedstx2only, two isolates (6.3%) possessed bothstx1andstx2, and two isolates (6.3%) possessedstx2c. Only three instances of indistinguishable pulsed-field gel electrophoresis patterns were identified. The age of the individuals from whom non-O157 VTEC were isolated ranged from eight months to 87 years. Mean and median ages were 30 and 22 years of age, respectively. Some areas of the province appeared to experience a higher than expected number of non-O157E coliin comparison with the number of stools that were received from these areas.CONCLUSIONS: The present study demonstrated a large number of infections associated with non-O157 VTEC in Manitoba. Most non-O157 cases appear to result from sporadic infections, and these occur typically in rural areas. Continued enhanced surveillance is necessary to understand the temporal patterns of non-O157 VTEC and the underlying epidemiological factors driving these patterns.

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Hussein, Hussein S., Brandolyn H. Thran, Mark R. Hall, William G. Kvasnicka, and Rodney C. Torell. "Verotoxin-Producing Escherichia coli in Culled Beef Cows Grazing Rangeland Forages." Experimental Biology and Medicine 228, no. 4 (April 2003): 352–57. http://dx.doi.org/10.1177/153537020322800404.

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The objective of this study was to assess prevalence of verotoxin-producing Escherichia coli (VTEC) in culled beef cows at the time of shipping to slaughter. Feces were collected from 82 cows on eight Nevada ranches during fall and winter (from September to January) after grazing rangeland forages. A random sample ( n = 154) of potential VTEC isolates were tested for verotoxicity and were screened for the presence (polymerase chain reaction) and expression (VTEC-reversed passive latex agglutination assay) of the toxin genes (i.e., VT1 and VT2). Seventeen isolates from four ranches were VTEC. Of these, four had the VT1 gene, five had the VT2 gene, seven had both genes, and one did not have either gene despite its toxicity to Vero cells. Except for one isolate (i.e., untypeable that reacted with VT1-latex beads without having VT1 gene), the genotype and phenotype data of the VTEC isolates matched. Another isolate (08:H– [nonmotile]) was verotoxic, but neither had nor expressed the toxin genes. Of the 17 isolates, four (from one cow) were O157:H7, 11 (from five cows on three ranches) were non-O157:H7 (two O8:H–, three O105:H–, three O116:H–, and three O141:H–), and two were untypeable. Because some of these VTEC serotypes (i.e., O8:H–, O141:H–, and O157:H7) are known to cause human illnesses, it is beneficial to identify VTEC-positive cows before slaughter. This is a critical step in any pre-or post-harvest strategy to minimize the risk of beef contamination with such pathogens.

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Mohd Asmawi, Ummi Mohlisi, Mohammad Nazmul Hasan Maziz, Mohammad Abdur Rashid, and Jamal Houssaini. "Human Behaviour and Responses Challenge towards Emergence of Infectious Diseases: E.coli clinical isolate." Environment-Behaviour Proceedings Journal 1, no. 1 (June 26, 2016): 146. http://dx.doi.org/10.21834/e-bpj.v1i1.208.

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Consumption of undercooked ground beef is the most common route of transmission of verotoxin-producing E.coli. It is estimated that non-O157 verotoxigenic E.coli (VTEC) can cause diarrhea.The sample was isolated from Universiti Malaya Medical Centre. All the isolates were identified using agarose gel electrophoresis method. This study aims to detect the verotoxin genes and detect the link or involvement of plasmids with these verotoxin genes. Therefore, this study will contribute to shed new light on resolving the significant and global problem of diarrheal disease caused by this particular pathogenic organism and help in improvising novel therapeutic approaches to improve human healthcare.© 2016. The Authors. Published for AMER ABRA by e-International Publishing House, Ltd., UK. Peer–review under responsibility of AMER (Association of Malaysian Environment-Behaviour Researchers), ABRA (Association of Behavioural Researchers on Asians) and cE-Bs (Centre for Environment-Behaviour Studies, Faculty of Architecture, Planning & Surveying, Universiti Teknologi MARA, Malaysia.Keywords: E.coli; non-0157; plasmid profile

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VERNOZY-ROZAND, C., C. MAZUY, S. RAY-GUENIOT, S. BOUTRAND-LOEÏ, A. MEYRAND, and Y. RICHARD. "Evaluation of the VIDAS Methodology for Detection of Escherichia coli O157 in Food Samples." Journal of Food Protection 61, no. 7 (July 1, 1998): 917–20. http://dx.doi.org/10.4315/0362-028x-61.7.917.

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An automated enzyme-linked fluorescence immunoassay (ELFA), the VIDAS E. coli O157 method, was compared with immunomagnetic separation (IMS) followed by culture on cefixime tellurite sorbitol MacConkey agar (CT-SMAC) for detecting Escherichia coli O157 in artificially and naturally contaminated food samples including raw milk cheeses, poultry, raw sausages, and ground beef retail samples. Confirmation of the samples positive according to the ELFA was performed by use of an automated immunoconcentration system, VIDAS ICE, which allows selective capture and release of target organisms. A total of 496 retail food samples were examined. Seventeen food samples gave positive values with the ELFA method, and among them 9 food samples were confirmed by the ICE method. Eight were shown to contain sorbitol-positive, O157-positive, H7-negative, motile, non-verotoxin-producing E. coli. The ninth positive sample contained an O157-positive, H7-negative, sorbitol-negative, non-verotoxin-producing E. coli. The IMS technique only allowed confirmation of this sorbitol-negative, non-verotoxin-producing E. coli O157.

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PALUMBO, SAMUEL A., JEFFREY E. CALL, FRANKIE J. SCHULTZ, and AARON C. WILLIAMS. "Minimum and Maximum Temperatures for Growth and Verotoxin Production by Hemorrhagic Strains of Escherichia coli." Journal of Food Protection 58, no. 4 (April 1, 1995): 352–56. http://dx.doi.org/10.4315/0362-028x-58.4.352.

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The influence of temperature on growth and verotoxin production by Escherichia coli strains was studied in brain heart infusion (BHI) broth both in shake cultures at various temperatures and in a temperature-gradient incubator. All strains of E. coli surveyed grew from at least 10 to 45°C, with some strains growing at 8° C. Verotoxin production (determined using the Vero cell–assay system) was a function of both temperature and time, with the highest titers produced at temperatures supporting the fastest growth (based on days to visible turbidity) and highest viable cell counts. However, for strains producing verotoxin, toxin production was detected at any temperature supporting growth. Three strains (of 16 tested) increased 1000-fold in viable count in 4 to 6 days at 10°C. The data presented here indicate that most E. coli strains surveyed can easily grow at ca. 10°C and thus suggest the potential for growth in temperature-abused refrigerated foods.

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30

Maloney, M., and C. A. Lingwood. "Interaction of Verotoxins with Glycosphingolipids." Trends in Glycoscience and Glycotechnology 5, no. 21 (1993): 23–31. http://dx.doi.org/10.4052/tigg.5.23.

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31

Krüger, Alejandra, Paula M. A. Lucchesi, and Alberto E. Parma. "Evaluation of vt2-subtyping methods for identifying vt2g in verotoxigenic Escherichia coli." Journal of Medical Microbiology 56, no. 11 (November 1, 2007): 1474–78. http://dx.doi.org/10.1099/jmm.0.47307-0.

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Verotoxin-producing Escherichia coli (VTEC) are important pathogens that can cause severe human disease, including haemorrhagic colitis and haemolytic–uraemic syndrome. A new variant of verotoxin, vt2g, has recently been described. It was possible to find this variant for the first time in Argentina among VTEC isolated from cattle. The present study evaluated the identification of this gene with three conventional methods used for subtyping the vt2 gene. The results show that it is possible to screen VTEC strains for the presence of vt2g without the implementation of new protocols.

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32

Pierard*, D. "Infections with Verotoxin-ProducingEscherichia Coli." Acta Clinica Belgica 47, no. 6 (January 1992): 387–96. http://dx.doi.org/10.1080/17843286.1992.11718260.

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33

Windler, Friederike, Hans Josef Weh, Dieter Kurt Hossfeld, Hans-Rüdiger Franz, Helge Karch, Jürgen Heesemann, and Rainer Laufs. "VEROTOXIN IN THROMBOTIC THROMBOCYTOPENIC PURPURA." European Journal of Haematology 42, no. 1 (April 24, 2009): 103. http://dx.doi.org/10.1111/j.1600-0609.1989.tb00256.x.

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34

Lingwood, C. A. "Verotoxin/Globotriaosyl Ceramide Recognition: Angiopathy, Angiogenesis and Antineoplasia." Bioscience Reports 19, no. 5 (October 1, 1999): 345–54. http://dx.doi.org/10.1023/a:1020299819637.

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Verotoxin (VT) is involved in the etiology of both hemorrhagic colitis and the hemolytic uremic syndrome which are microvasculopathies of the colon and pediatric renal glomerulus respectively. Thus, VT can be considered a vasotoxin. Cell sensitivity in vitro varies according to the receptor glycolipid (globotriaosyl ceramide-Gb3) expression and also to intracellular trafficking of the receptor/toxin complex, such that in highly sensitive cells, the toxin is targeted to the endoplasmic reticulum and nuclear envelope. Such cells include tumor cells which have become drug resistant. Thus Gb3 is upregulated in certain tumors and when such tumor cells become drug resistant, their sensitivity to verotoxin increases. This may be due to a direct role of the MDR1 drug efflux pump in glycolipid biosynthesis. In addition to the tumor tissue, the toxin receptor may also be expressed in the tumor neovasculature suggesting that activated endothelial cells may be verotoxin sensitive. Thus VT may have both a direct and indirect antineoplastic potential. VT has proved highly effective in a xenograft cancer model and the possible therapeutic use of VT is discussed.

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35

Itoh, Kunihiko, Takehiko Tezuka, Kazuyuki Inoue, Hitoshi Tada, and Toshio Suzuki. "Different Binding Property of Verotoxin-1 and Verotoxin-2 Against Their Glycolipid Receptor, Globotriaosylceramide." Tohoku Journal of Experimental Medicine 195, no. 4 (2001): 237–43. http://dx.doi.org/10.1620/tjem.195.237.

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36

Barnett Foster, Debora, Maan Abul-Milh, Mario Huesca, and Clifford A. Lingwood. "Enterohemorrhagic Escherichia coliInduces Apoptosis Which Augments Bacterial Binding and Phosphatidylethanolamine Exposure on the Plasma Membrane Outer Leaflet." Infection and Immunity 68, no. 6 (June 1, 2000): 3108–15. http://dx.doi.org/10.1128/iai.68.6.3108-3115.2000.

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ABSTRACT Enterohemorrhagic Escherichia coli (EHEC) is a gastrointestinal pathogen that causes watery diarrhea and hemorrhagic colitis and can lead to serious and even fatal complications such as hemolytic uremic syndrome. We investigated the ability of EHEC to kill host cells using three human epithelial cell lines. Analysis of phosphatidylserine expression, internucleosomal cleavage of host cell DNA and morphological changes detected by electron microscopy changes revealed evidence of apoptotic cell death. The rates and extents of cell death were similar for both verotoxin-producing and nonproducing strains of EHEC as well as for a related gastrointestinal pathogen, enteropathogenic E. coli (EPEC). The induction of apoptosis by bacterial attachment was independent of verotoxin production and greater than that produced by a similar treatment with verotoxin alone. Expression of phosphatidylethanolamine, previously reported to bind EHEC and EPEC, was also increased on apoptotic cells but with little correlation to phosphatidylserine expression. Phosphatidylethanolamine levels but not phosphatidylserine levels on dying cells correlated with EHEC binding. Cells treated with phosphatidylethanolamine-containing liposomes also showed increased EHEC binding. These results suggest that bacterial induction of apoptosis offers an advantage for bacterial attachment by augmenting outer leaflet levels of the phosphatidylethanolamine receptor.

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37

Speirs, Joan I., and Mumtaz Akhtar. "Detection of Escherichia coli cytotoxins by enzyme-linked immunosorbent assays." Canadian Journal of Microbiology 37, no. 8 (August 1, 1991): 650–53. http://dx.doi.org/10.1139/m91-110.

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Sandwich enzyme-linked immunosorbent assays (ELISAs) were developed to detect Escherichia coli cytotoxins. Wells were coated with monoclonal antibodies from hybridomas 13C4 and (or) 11E10, and biotin conjugates of these antibodies were used for detecting verotoxin 1 and Shiga-like toxin II, respectively. Sensitivities were about 100 and 200 cytotoxic doses, respectively. Verotoxin 2 was detected by ELISA with monoclonal antibody 11E10, but at a sensitivity of only about 4000 cytotoxic doses. ELISA results of polymyxin-treated cell extracts from cultures of 67 E. coli strains were in agreement with Vero cell assay as regards the presence and type of toxin. Key words: Escherichia coli, cytotoxin, ELISA.

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38

Ramotar, K., E. Henderson, R. Szumski, and T. J. Louie. "Impact of free verotoxin testing on epidemiology of diarrhea caused by verotoxin-producing Escherichia coli." Journal of clinical microbiology 33, no. 5 (1995): 1114–20. http://dx.doi.org/10.1128/jcm.33.5.1114-1120.1995.

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39

Karmali, M. A., M. Petric, S. Louie, and R. Cheung. "ANTIGENIC HETEROGENEITY OF ESCHERICHIA COLI VEROTOXINS." Lancet 327, no. 8473 (January 1986): 164–65. http://dx.doi.org/10.1016/s0140-6736(86)92307-x.

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40

HEREDIA, NORMA, MARCO ESCOBAR, CRISTINA RODRÍGUEZ-PADILLA, and SANTOS GARCÍA. "Extracts of Haematoxylon brasiletto Inhibit Growth, Verotoxin Production, and Adhesion of Enterohemorrhagic Escherichia coli O157:H7 to HeLa Cells." Journal of Food Protection 68, no. 7 (July 1, 2005): 1346–51. http://dx.doi.org/10.4315/0362-028x-68.7.1346.

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The extracts of 33 plants were evaluated for their effects on growth of Escherichia coli O157:H7 (EHEC). The extract of Haematoxylon brasiletto was the only one that effectively inhibited bacterial growth. The effects of ethanolic extracts of this plant on growth, verotoxin production, and adhesion of E. coli O157:H7 to HeLa cells were determined. The MBC for growth was 4 mg/ml. No verotoxin formation was detected at 1, 2, or 3 mg/ml. Preexposing bacteria and HeLa cells to various concentrations of extracts affected the adhesion between non-EHEC and HeLa cells. Partial purification of the active fraction suggested that polyphenols might play a role in the antimicrobial activity exhibited by H. brasiletto extracts.

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41

Rock, Gail, William Clark, Marion Sternbach, Maria Kolajova, and Peter McLaine. "Hemolytic Uremic Syndrome Is an Immune Mediated Disease: Role of Anti-CD36 Antibodies." Blood 106, no. 11 (November 16, 2005): 3990. http://dx.doi.org/10.1182/blood.v106.11.3990.3990.

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Abstract Hemolytic uremic syndrome is a disorder in which platelet microthrombi are formed which have a particular propensity to deposit in the kidney microvasculature resulting in impaired renal function and thrombocytopenia. The mechanism of formation of these microthrombi is not known. In this study, we showed that plasma from five adult and six pediatric cases of HUS caused aggregation and release of adenosine triphosphate from normal platelets. The plasma reacted against platelet lysate in a protein blot and all samples showed reactivity against a band at 88kDa corresponding to the membrane antigen CD36. This was confirmed by probing with Mo91, a monoclonal antibody to CD36. CD36 was also identified in the immune complex formed by incubation of patient plasmas with normal platelet lysate. In other studies, bands of 32kDa and 7.7kDa were obtained when purified verotoxin was protein blotted and probed with either patient plasma or with anti-CD36 antibody Mo91 suggesting structural homologies between CD36 and verotoxin. The data support the concept of an immunological pathogenesis for HUS and suggest that molecular mimicry involving one or both of the homologous domains in membrane-bound CD36 and verotoxin lead to the development of antibodies capable of inducing the pathophysiological events characteristic of HUS.

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42

&NA;. "Verotoxin induces apoptosis in tumour cells." Inpharma Weekly &NA;, no. 915 (November 1993): 12. http://dx.doi.org/10.2165/00128413-199309150-00024.

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43

Maniar, A. C., T. Williams, C. M. Anand, and G. W. Hammond. "Detection of verotoxin in stool specimens." Journal of Clinical Microbiology 28, no. 1 (1990): 134–35. http://dx.doi.org/10.1128/jcm.28.1.134-135.1990.

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44

OHARA, Tatsuki, Seiichi KOJIO, Hui-Min ZHANG, Fumitake GEJYO, and Tatsuo YAMAMOTO. "Protective Effect of Azithromycin against Verotoxin." Journal of the Japanese Association for Infectious Diseases 76, no. 2 (2002): 126–28. http://dx.doi.org/10.11150/kansenshogakuzasshi1970.76.126.

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45

HARING, V., and P. DESMARCHELIER. "Verotoxin-producing E coli in sheep." Australian Veterinary Journal 75, no. 9 (September 1997): 675–76. http://dx.doi.org/10.1111/j.1751-0813.1997.tb15373.x.

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46

Lingwood, C. A. "Verotoxin-Binding in Human Renal Sections." Nephron 66, no. 1 (1994): 21–28. http://dx.doi.org/10.1159/000187761.

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47

LINGWOOD, C. "Role of verotoxin receptors in pathogenesis." Trends in Microbiology 4, no. 4 (April 1996): 147–53. http://dx.doi.org/10.1016/0966-842x(96)10017-2.

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48

Gerritzen, A. "Vergleichender Verotoxin-Nachweis im Stuhl mit zwei Enzymimmunoassays und dem Zytotoxizitätstest auf Verozellen - Comparison of Two Enzyme Immuno Assays and Verocell Cytotoxicity for Detection of Verotoxins in Human Feces." LaboratoriumsMedizin 22, no. 12 (January 1998): 704–13. http://dx.doi.org/10.1515/labm.1998.22.12.704.

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49

Peter, M. G., and C. A. Lingwood. "Apparent cooperativity in multivalent verotoxin-globotriaosyl ceramide binding: kinetic and saturation binding studies with [125I]verotoxin." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1501, no. 2-3 (June 2000): 116–24. http://dx.doi.org/10.1016/s0925-4439(00)00011-9.

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50

Tam, Patty, Radhia Mahfoud, Anita Nutikka, Aye Aye Khine, Beth Binnington, Paul Paroutis, and Clifford Lingwood. "Differential intracellular transport and binding of verotoxin 1 and verotoxin 2 to globotriaosylceramide‐containing lipid assemblies." Journal of Cellular Physiology 216, no. 3 (September 2008): 750–63. http://dx.doi.org/10.1002/jcp.21456.

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Journal articles on the topic 'Verotoxine'

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