Glycolipid binding of purified and recombinant Escherichia coli produced verotoxin in vitro.

Lingwood, Clifford A.; Law, Helen K. W.; Richardson, Susan E.; Petric, Martin; Brunton, James; Grandis, S De; Karmali, M A

doi:10.1016/s0021-9258(18)47490-x

Cited by 416 publications

(66 citation statements)

References 28 publications

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“…In our histochemical study, the presence of immunoreactions to VT2v in lysosomes of pyramidal cells suggests that VT2v may be taken up by neuron fibers and axonally transported to their cell bodies. The glycolipid globotriosyl ceramide is a binding receptor for VT1 and VT2 (16,41). Galabiosyl ceramide also binds to VT1, and the glycolipid was detected in the rabbit central nervous system (48).…”

Section: Discussionmentioning

confidence: 99%

Direct evidence of neuron impairment by oral infection with verotoxin-producing Escherichia coli O157:H- in mitomycin-treated mice

et al. 1994

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We developed a mouse model of acute encephalopathy induced by verotoxin 2 variant (VT2v)-producing Escherichia coli. Three-week-old mice were inoculated intragastrically with approximately 10(10) CFU of E. coli O157:H- strain E32511/HSC and simultaneously given an intraperitoneal injection of mitomycin (MMC; 2.5 mg/kg). Drinking water containing 5 g of streptomycin sulfate per liter was given ad libitum from 3 days before the infection. From 1 to 2 days after bacterial inoculation, clinical features including weight loss, weakness, and flaccid paralysis of the extremities developed, usually culminating in death within 4 days. Diarrhea was not observed during the course of disease. No mice died in the absence of streptomycin or MMC treatment for 2 weeks after the oral bacterial infection. Judging from the clinical course and the biochemical and histological examination, the cause of death was not likely to be attributable to renal failure or to a side effect of MMC. To better understand the cause of death, we examined the brain cortex and spinal cord of the moribund mice by electron microscopy. Mice showing mortal symptoms were given horseradish peroxidase intravenously. The tracer was present in the endothelial basal lamina, in the surrounding extracellular spaces, and even in the neuron fibers of the brain cortex. Furthermore, immunoreactivity of VT2v, proved by the use of rabbit anti-VT2 serum, was localized selectively in the damaged myelin sheaths of neuron fibers which were accompanied by edematous axons in the brain cortex and spinal cord. These findings strongly suggest that VT2v is toxic to both endothelial cells and neurons in the central nervous system and subsequently causes fatal acute encephalopathy.

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Section: Discussionmentioning

confidence: 99%

Direct evidence of neuron impairment by oral infection with verotoxin-producing Escherichia coli O157:H- in mitomycin-treated mice

et al. 1994

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“…Inhibition of Toxin-Binding Shigatoxigenic Escherichia coli produce Stx type 1 as well as type 2. The pentamer subunit of Stx, termed StxB interacts with a number host cell surface constituents, the main one globotriaosylceramide (Gb3), for epithelial cell internalization [190,191]. The Gb3 receptor is a lipid-conjugated oligosaccharide structure consisting of a Galα1,4Galβ1,4Glc trisaccharide [192].…”

Section: Adhesion Inhibitionmentioning

confidence: 99%

Anti-Pathogenic Functions of Non-Digestible Oligosaccharides In Vitro

et al. 2020

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Non-digestible oligosaccharides (NDOs), complex carbohydrates that resist hydrolysis by salivary and intestinal digestive enzymes, fulfill a diversity of important biological roles. A lot of NDOs are known for their prebiotic properties by stimulating beneficial bacteria in the intestinal microbiota. Human milk oligosaccharides (HMOs) represent the first prebiotics that humans encounter in life. Inspired by these HMO structures, chemically-produced NDO structures (e.g., galacto-oligosaccharides and chito-oligosaccharides) have been recognized as valuable food additives and exert promising health effects. Besides their apparent ability to stimulate beneficial microbial species, oligosaccharides have shown to be important inhibitors of the development of pathogenic infections. Depending on the type and structural characteristics, oligosaccharides can exert a number of anti-pathogenic effects. The most described effect is their ability to act as a decoy receptor, thereby inhibiting adhesion of pathogens. Other ways of pathogenic inhibition, such as interference with pathogenic cell membrane and biofilm integrity and DNA transcription, are less investigated, but could be equally impactful. In this review, a comprehensive overview of In vitro anti-pathogenic properties of different NDOs and associated pathways are discussed. A framework is created categorizing all anti-pathogenic effects and providing insight into structural necessities for an oligosaccharide to exert one of these effects.

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“…79,80,83,86 Furthermore, P k is the receptor for Shiga toxin from Shigella dysenteriae (Stx) or certain E. coli strains (Stx1 and Stx2) on renal epithelium, platelets, and endothelium. 81,82 A disease connected to the P k antigen is Fabry disease, in which deficiency of the lysosomal enzyme α-galactosidase A causes accumulation of sphingolipids, mainly P k , in some cell types and body fluids. 87 It has been shown that mice with Fabry disease are protected against Stx from enterohemorrhagic E. coli (EHEC).…”

Section: Bacteriamentioning

confidence: 99%

P1PK: The blood group system that changed its name and expanded

et al. 2013

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The antigens in the P1PK blood group system are carried on glycosphingolipids. The system currently includes three different antigens, P1, Pk, and NOR. The P1 antigen was disovered in 1927 by Landsteiner and Levine, and Pkand NOR were described in 1951 and 1982, respectively. As in the ABO system, naturally occurring antibodies of the immunoglobulin (Ig) M or IgG class, against the missing carbohydrate structures, can be present in the sera of people lacking the corresponding antigen. Anti-P1 is generally a weak and cold-reactive antibody not implicated in hemolytic transfusion reaction (HTR) or hemolytic disease of the fetus and newborn while Pkantibodies can cause HTR, and anti-NOR is regarded as a polyagglutinin. A higher frequency of miscarriage is seen in women with the rare phenotypes p, P1 k, and P2 k. Furthermore, the Pkand P1 antigens have wide tissue distributions and can act as host receptors for various pathogens and toxins. Why p individuals lack not only Pkand P expression but also P1 has been a longstanding enigma. Recently, it was shown that the same A4GALT-encoded galactosyltransferase synthesizes both the P1 and Pkantigens and that a polymorphism in a new exon in this gene predicts the P1and P2phenotypes. Immunohematology 2013;29:25–33.

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Glycolipid binding of purified and recombinant Escherichia coli produced verotoxin in vitro.

Cited by 416 publications

References 28 publications

Direct evidence of neuron impairment by oral infection with verotoxin-producing Escherichia coli O157:H- in mitomycin-treated mice

Direct evidence of neuron impairment by oral infection with verotoxin-producing Escherichia coli O157:H- in mitomycin-treated mice

Anti-Pathogenic Functions of Non-Digestible Oligosaccharides In Vitro

P1PK: The blood group system that changed its name and expanded

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