Search results for "Enterotoxins"

showing 10 items of 49 documents

Congenital secretory diarrhoea caused by activating germline mutations in GUCY2C

2016

Objective Congenital sodium diarrhoea (CSD) refers to a form of secretory diarrhoea with intrauterine onset and high faecal losses of sodium without congenital malformations. The molecular basis for CSD remains unknown. We clinically characterised a cohort of infants with CSD and set out to identify disease-causing mutations by genome-wide genetic testing. Design We performed whole-exome sequencing and chromosomal microarray analyses in 4 unrelated patients, followed by confirmatory Sanger sequencing of the likely disease-causing mutations in patients and in their family members, followed by functional studies. Results We identified novel de novo missense mutations in GUCY2C, the gene encod…

DiarrheaMale0301 basic medicinemedicine.medical_specialtyReceptors PeptideColonGuanylinGuanosine MonophosphateMutation MissenseReceptors EnterotoxinGUANYLATE CYCLASEBiologyCHRONIC DIARRHOEAPathogenesis03 medical and health scienceschemistry.chemical_compoundsymbols.namesakeGermline mutationInternal medicineBACTERIAL ENTEROTOXINSmedicineHumansMissense mutationAbnormalities MultipleGenetic Predisposition to Disease1506Intestinal MucosaCyclic guanosine monophosphateSanger sequencingPAEDIATRIC DIARRHOEASodiumGastroenterologyInfantMolecular Reproduction Development & Genetics (formed by the merger of DBGL and CRBME)Molecular biologyIntestines030104 developmental biologyEndocrinologyIntestinal AbsorptionReceptors Guanylate Cyclase-CoupledchemistryINTESTINAL ION TRANSPORTsymbolsFemaleMetabolism Inborn ErrorsIntracellularUroguanylinGut
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Toxin production by Campylobacter spp

1997

Of all the virulence factors that were proposed for Campylobacter jejuni and related species to cause disease in humans, the discovery of toxin production was the most promising but led to a rather confusing and even disappointing stream of data. The discussion of whether proteinaceous exotoxins are relevant in disease remains open. One important reason for this lack of consensus is the anecdotal nature of the literature reports. To provide a basis for an unbiased opinion, this review compiles all described exotoxins, compares their reported properties, and provides a summary of animal model studies and clinical data. The toxins are divided into enterotoxins and cytotoxins and are sorted ac…

DiarrheaMicrobiology (medical)GeneticsVirulenceGeneral Immunology and MicrobiologyCytotoxinsEpidemiologyToxinCampylobacterCampylobacteraceaePublic Health Environmental and Occupational HealthVirulenceCampylobacterEnterotoxinBiologymedicine.disease_causebiology.organism_classificationCampylobacter jejuniMicrobiologyEnterotoxinsInfectious DiseasesAnimal modelmedicineProspective StudiesResearch ArticleClinical Microbiology Reviews
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Protection from experimental allergic encephalomyelitis by application of a bacterial superantigen

1992

Certain bacterial and viral T cell stimulating proteins ('superantigens') are known to be very potent activators of T cells with certain V beta receptors. When applied in vivo these molecules induce anergy in those T cells responding to them. In this study we have investigated the influence of staphylococcal enterotoxins (SE) on myelin basic protein (MBP)-specific T cells in Lewis rats. As MBP-specific T cells in rats belong exclusively to the V beta 8.2+ CD4+ subset, the induction of experimental allergic encephalomyelitis (EAE) allows for an estimation of the functional state of the respective V beta-bearing T cells after enterotoxin-induced activation. In vitro, various MBP-specific T ce…

Encephalomyelitis Autoimmune ExperimentalT-LymphocytesEncephalomyelitisT cellImmunologyBiologyLymphocyte ActivationCell LineImmune toleranceEnterotoxinsAntigenImmune TolerancemedicineSuperantigenAnimalsImmunology and AllergyAntigens BacterialExperimental autoimmune encephalomyelitisGeneral MedicineT lymphocytemedicine.diseaseRatsMyelin basic proteinmedicine.anatomical_structureRats Inbred LewImmunologybiology.proteinFemaleInternational Immunology
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Characterization of polymorphisms in the toxin A and B genes of Clostridium difficile.

2006

We have used six independent polymerase chain reactions (A1–A3 and B1–B3) for amplification of the entire sequence of the two toxin genes tcdA and tcdB of several Clostridium difficile strains. With this approach we have detected (1) restriction site polymorphisms which are distributed all over the genes, and (2) deletions that could be found only in tcdA. Characteristic differences between strains were mainly focused to the 5′ third of tcdB (B1 fragment) and/or the 3′ third of tcdA (A3 fragment). The possible use of our approach for typing of C. difficile toxin genes is discussed.

GeneticsPolymorphism GeneticClostridioides difficileBacterial ToxinsClostridium difficile toxin AClostridium difficile toxin BBiologyClostridium difficileMicrobiologyMolecular biologyPolymerase Chain Reactionlaw.inventionRestriction siteEnterotoxinsBacterial ProteinslawGenes BacterialGenotypeGeneticsTypingRestriction fragment length polymorphismMolecular BiologyPolymerase chain reactionPolymorphism Restriction Fragment LengthFEMS microbiology letters
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Prevention and reversal of superantigen-induced anergy by contact allergen exposure

1995

The superantigen Staphylococcal enterotoxin B (SEB) and the contact allergen 2,4-dinitrofluorbenzene (DNFB) both react with V beta 8+ T-cells delivering distinct signals. Pre-treatment with DNFB painted onto the same skin site where SEB was to be injected, prevented the induction of anergy in V beta + T-cells that was otherwise induced after SEB had been injected intradermally over a period of 2 weeks. Application of the irritant sodium dodecyl sulfate (SDS) instead of DNFB did not exert this effect. Application of DNFB at a site distant from the site where SEB was injected resulted in a much weaker inhibitory influence on the induction of anergy by SEB. Established anergy of V beta 8+ T-ce…

Interleukin 2Cell typeAdministration TopicalReceptors Antigen T-Cell alpha-betaT-Lymphocyteschemical and pharmacologic phenomenaDermatologyEnterotoxinDermatitis Contactmedicine.disease_causeBiochemistryEnterotoxinsMicechemistry.chemical_compoundAllergenImmune TolerancemedicineSuperantigenAnimalsSodium dodecyl sulfateBeta (finance)Molecular BiologyMice Inbred BALB CSuperantigenshemic and immune systemsAllergensbiological factorsIn vitrochemistryImmunologyDinitrofluorobenzeneFemalemedicine.drugExperimental Dermatology
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Clostridium difficile toxins A and B inhibit human immune response in vitro

1988

Two Clostridium difficile toxins isolated from strain VPI 10463 were tested for their effect on different human T-cell proliferation systems. In mitogen- and antigen-driven T-cell proliferation systems, toxins inhibited the proliferative response in a dose-dependent fashion. In interleukin-2-driven culture systems, no effect of toxins could be found on preactivated T cells. We suspected that monocytes were the influenced cells, since in antigen- and mitogen-driven systems monocytes were necessary for the proliferative response, whereas the interleukin-2-driven system was independent of monocytes. To prove this concept, purified monocytes were treated with toxins. The treatment was found to …

Interleukin 2Cellular immunityT-LymphocytesBacterial ToxinsImmunologyEnterotoxinIn Vitro TechniquesBiologyLymphocyte ActivationMicrobiologyMonocytesMicrobiologyEnterotoxinsImmune systemBacterial ProteinsAntigenmedicineHumansMonocytePseudomembranous colitisClostridium difficileInfectious Diseasesmedicine.anatomical_structureInterleukin-2ParasitologyMitogensResearch Articlemedicine.drugInfection and Immunity
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Distribution and kinetics of superantigen-induced cytokine gene expression in mouse spleen.

1993

The polyclonal stimulation of T cells by bacterial superantigens is involved in the pathogenesis of the toxic shock syndrome in certain staphylococcal and streptococcal infections. Here we describe the onset and kinetics of superantigen-induced cytokine production in situ in spleens of normal BALB/c mice monitored at the level of cytokine mRNA expression by in situ hybridization. Messenger RNAs for interleukin 2 (IL-2), interferon gamma, and tumor necrosis factors (TNF) alpha and beta were not expressed at detectable levels in spleens of unstimulated animals but became visible already 30 min after intraperitoneal application of 50 micrograms staphylococcal enterotoxin B. All mRNA levels sho…

Interleukin 2LipopolysaccharidesSalmonella typhimuriumStaphylococcus aureusInterferon type IITranscription Geneticmedicine.medical_treatmentT cellT-LymphocytesImmunologyGene ExpressionBiologyEnterotoxinsMiceAldesleukinGene expressionmedicineSuperantigenImmunology and AllergyAnimalsInterferon gammaRNA MessengerIn Situ HybridizationMice Inbred BALB CSuperantigensTumor Necrosis Factor-alphaMacrophagesArticlesMolecular biologyKineticsCytokinemedicine.anatomical_structureCytokinesInterleukin-2Spleenmedicine.drugThe Journal of experimental medicine
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Rotavirus 2/6 virus-like particles administered intranasally in mice, with or without the mucosal adjuvants cholera toxin and Escherichia coli heat-l…

2001

ABSTRACTWe investigated the rotavirus-specific lymphocyte responses induced by intranasal immunization of adult BALB/c mice with rotavirus 2/6 virus-like particles (2/6-VLPs) of the bovine RF strain, by assessing the profile of cytokines produced after in vitro restimulation and serum and fecal antibody responses. The cytokines produced by splenic cells were first evaluated. Intranasal immunization with 50 μg of 2/6-VLPs induced a high serum antibody response, including immunoglobulin G1 (IgG1) and IgG2a, a weak fecal antibody response, and a mixed Th1/Th2-like profile of cytokines characterized by gamma interferon and interleukin 10 (IL-10) production and very low levels of IL-2, IL-4, and…

Interleukin 2RotavirusCholera ToxinLymphocyteImmunologyBacterial ToxinsBiologymedicine.disease_causeMicrobiologyMicrobiology03 medical and health sciencesEnterotoxinsInterferon-gammaMiceImmune systemTh2 CellsAdjuvants ImmunologicVirologyChlorocebus aethiopsmedicineAnimalsInterferon gammaInterleukin 5Administration Intranasal030304 developmental biology[SDV.MP.VIR] Life Sciences [q-bio]/Microbiology and Parasitology/Virology0303 health sciencesMice Inbred BALB C030306 microbiologyToxinEscherichia coli ProteinsCholera toxinVirionTh1 Cells3. Good healthVIROLOGIEmedicine.anatomical_structureImmunizationInsect Science[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyImmunologyPathogenesis and ImmunityCytokinesInterleukin-2FemaleImmunizationInterleukin-5medicine.drug
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Modulation of Contact Sensitivity Responses by Bacterial Superantigen

1995

Superantigens are potent modulators of the immune system, especially T cells. Therefore, we determined the influence of superantigens on the T-cell-mediated immune response, contact sensitivity. We chose the combination of staphylococcal enterotoxin B (SEB) as superantigen and 2,4-dinitrofluorbenzene (DNFB) as the contact sensitizer, because in BALB/c mice SEB reacts almost exclusively with V beta 8+ T cells, and these cells are capable of transferring contact sensitivity to DNFB from sensitized donors to naive syngeneic recipients. Pretreatment with a single intradermal injection of 50 ng SEB 24 h before DNFB exposure at the same site on the lower abdomen enhanced the induction of contact …

Lymphoid Tissue24-dinitrofluorbenzeneReceptors Antigen T-Cell alpha-betaT-LymphocytesDown-Regulationchemical and pharmacologic phenomenaDermatologyEnterotoxinDermatitis Contactcontact sensitivityBacterial superantigenBiochemistrysuperantigenProinflammatory cytokineEnterotoxinsInterferon-gammaMiceImmune systemmedicineSuperantigenAnimalsIntradermal injectionMolecular BiologySensitizationSkinAntigens BacterialMice Inbred BALB CSuperantigensbusiness.industryhemic and immune systemsCell BiologyContact sensitivitybiological factorsStaphylococcal enterotoxin Bmedicine.anatomical_structureImmunologyDinitrofluorobenzeneFemaleImmunizationbusinessJournal of Investigative Dermatology
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Variant toxin B and a functional toxin A produced by Clostridium difficile C34.

2001

A particular property of Clostridium difficile strain C34 is an insertion of approximately 2 kb in the tcdA-C34 gene that does not hinder expression of a fully active TcdA-C34 molecule. Intoxication with TcdA-C34 induced an arborized appearance in eukaryotic cells (D-type cytopathic effect); intoxication with TcdB-C34 induced a spindle-like appearance of cells (S-type cytopathic effect). Inactivation of GTPases with purified toxins revealed that Rho, Rac, Cdc42, and Rap are substrates of TcdA-C34. The variant cytotoxin TcdB-C34 inactivated Rho, Rac, Cdc42, Rap, Ral, and R-Ras. Hence, this is the first ‘S-type’ cytotoxin which inactivates both Rho and R-Ras, and is coexpressed with a ‘D-type…

MaleCell SurvivalBacterial ToxinsClostridium difficile toxin AClostridium difficile toxin BGTPaseEnterotoxinCHO CellsBiologymedicine.disease_causeMicrobiologyMicrobiologyEnterotoxinsBacterial ProteinsCricetinaeGeneticsmedicineAnimalsHumansMolecular BiologyCells CulturedCytopathic effectSkinToxinClostridioides difficileCytotoxinsGenetic VariationClostridium difficileMolecular biologyCdc42 GTP-Binding ProteinDNA Transposable ElementsMicroscopy Electron ScanningFEMS microbiology letters
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