Search results for "Dextran sulfate"

showing 10 items of 38 documents

Blood flow patterns spatially associated with platelet aggregates in murine colitis.

2009

In the normal murine mucosal plexus, blood flow is generally smooth and continuous. In inflammatory conditions, such as chemically-induced murine colitis, the mucosal plexus demonstrates markedly abnormal flow patterns. The inflamed mucosal plexus is associated with widely variable blood flow velocity as well as discontinuous and even bidirectional flow. To investigate the mechanisms responsible for these blood flow patterns, we used intravital microscopic examination of blood flow within the murine mucosal plexus during dextran sodium sulphate-and trinitrobenzenesulfonic acid-induced colitis. The blood flow patterns within the mucosal plexus demonstrated flow exclusion in 18% of the vessel…

Blood PlateletsPathologymedicine.medical_specialtyHistologyPlatelet AggregationInterleukin-1betaBiologyArticleMicrocirculationchemistry.chemical_compoundMiceIntestinal mucosamedicineAnimalsPlateletColitisIntestinal MucosaEcology Evolution Behavior and SystematicsPlexusMice Inbred BALB CGene Expression ProfilingMicrocirculationDextran SulfateBlood flowmedicine.diseaseColitisMice Inbred C57BLDextranchemistryTrinitrobenzenesulfonic AcidRegional Blood FlowAcute DiseaseEndothelium VascularAnatomyChemokinesIntravital microscopyBiotechnologyAnatomical record (Hoboken, N.J. : 2007)
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Perforin deficiency attenuates inflammation and tumor growth in colitis-associated cancer

2010

Background: Patients with inflammatory bowel disease (IBD) have a markedly increased risk to develop colon cancer, but there are only limited data about the host antitumor response in such colitis-associated cancer. In the present study we aimed at assessing the role of perforin-dependent effector mechanisms in the immune response in a murine model of colitis-associated colon cancer. Methods: Wildtype and perforin-deficient mice were analyzed in a mouse model of colitis-associated colon cancer using azoxymethane (AOM) and dextran sodium sulfate (DSS). Results: Tumors of wildtype mice showed infiltration of CD4+, CD8+ T cells, natural killer (NK) cells, high numbers of apoptotic cells, and e…

CD4-Positive T-LymphocytesCytotoxicity ImmunologicPore Forming Cytotoxic ProteinsT-LymphocytesMedizinInflammationCD8-Positive T-LymphocytesBiologymedicine.disease_causeInflammatory bowel diseaseMiceImmune systemmedicineAnimalsImmunology and AllergyCytotoxic T cellIntestinal MucosaColitisReverse Transcriptase Polymerase Chain ReactionPerforin DeficiencyDextran SulfateGastroenterologyColitismedicine.diseaseSpecific Pathogen-Free OrganismsKiller Cells NaturalMice Inbred C57BLDisease Models AnimalPerforinChronic DiseaseColonic NeoplasmsImmunologybiology.proteinmedicine.symptomCarcinogenesisInflammatory Bowel Diseases
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Mast Cells Infiltrating Inflamed or Transformed Gut Alternatively Sustain Mucosal Healing or Tumor Growth.

2015

Abstract Mast cells (MC) are immune cells located next to the intestinal epithelium with regulatory function in maintaining the homeostasis of the mucosal barrier. We have investigated MC activities in colon inflammation and cancer in mice either wild-type (WT) or MC-deficient (KitW-sh) reconstituted or not with bone marrow-derived MCs. Colitis was chemically induced with dextran sodium sulfate (DSS). Tumors were induced by administering azoxymethane (AOM) intraperitoneally before DSS. Following DSS withdrawal, KitW-sh mice showed reduced weight gain and impaired tissue repair compared with their WT littermates or KitW-sh mice reconstituted with bone marrow-derived MCs. MCs were localized i…

Cancer ResearchPathologyColorectal cancerCell CountAnimals; Animals Congenic; Azoxymethane; Carcinoma; Cell Count; Cell Transformation Neoplastic; Cells Cultured; Colitis; Colonic Neoplasms; Dextran Sulfate; Epithelial Cells; Humans; Inflammatory Bowel Diseases; Interleukin-33; Intestinal Mucosa; Mast Cells; Mice; Mice Inbred C57BL; Mice Knockout; Models Biological; Proto-Oncogene Proteins c-kit; Receptors Interleukin; Regeneration; Serine Endopeptidases; Species Specificity; Specific Pathogen-Free Organisms; Cancer Research; Oncology; Medicine (all)chemistry.chemical_compoundMiceAnimals CongenicMast CellMast CellsIntestinal MucosaCells CulturedMice KnockoutColonic NeoplasmMedicine (all)Dextran SulfateSerine EndopeptidasesColitisIntestinal epitheliumSpecific Pathogen-Free OrganismsSerine EndopeptidaseProto-Oncogene Proteins c-kitCell Transformation NeoplasticOncologyColonic Neoplasmsmedicine.symptomHumanmedicine.medical_specialtyAzoxymethaneInflammationModels BiologicalImmune systemSpecies SpecificitymedicineSpecific Pathogen-Free OrganismAnimalsHumansRegenerationColitisEpithelial CellAnimalAzoxymethanebusiness.industryInflammatory Bowel DiseaseCarcinomaEpithelial CellsReceptors Interleukinmedicine.diseaseInflammatory Bowel DiseasesInterleukin-33Interleukin-1 Receptor-Like 1 ProteinMice Inbred C57BLchemistrybusinessWound healingColitiHomeostasisCancer research
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Vascular Microarchitecture of Murine Colitis-Associated Lymphoid Angiogenesis

2009

In permissive tissues, such as the gut and synovium, chronic inflammation can result in the ectopic development of anatomic structures that resemble lymph nodes. These inflammation-induced structures, termed lymphoid neogenesis or tertiary lymphoid organs, may reflect differential stromal responsiveness to the process of lymphoid neogenesis. To investigate the structural reorganization of the microcirculation involved in colonic lymphoid neogenesis, we studied a murine model of dextran sodium sulfate (DSS)-induced colitis. Standard 2-dimensional histology demonstrated both submucosal and intramucosal lymphoid structures in DSS-induced colitis. A spatial frequency analysis of serial histolog…

Colitis LymphocyticPathologymedicine.medical_specialtyHistologyStromal cellLymphoid TissueAngiogenesisBiologyArticleMicrocirculationMicemedicineAnimalsIntestinal MucosaColoring AgentsEcology Evolution Behavior and SystematicsMicrodissectionMicroscopy ConfocalNeovascularization PathologicStaining and LabelingMicrocirculationDextran SulfateHistologyMatrix MetalloproteinasesCapillariesMice Inbred C57BLDisease Models AnimalLymphatic systemRegional Blood FlowCytokinesLymphChemokinesAnatomyIntravital microscopyBiotechnologyThe Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology
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An inducible mouse model of colon carcinogenesis for the analysis of sporadic and inflammation-driven tumor progression.

2007

Colorectal cancer is a life-threatening disease that can develop spontaneously or as a complication of inflammatory bowel diseases. Mouse models are essential tools for the preclinical testing of novel therapeutic options in vivo. Here, we provide a highly reliable protocol for an experimental mouse model to study the development of colon cancers. It is based on the mutagenic agent azoxymethane (AOM), which exerts colonotropic carcinogenicity. Repeated intraperitoneal administration of AOM results in the development of spontaneous tumors within 30 weeks. As an alternative option, inflammation-dependent tumor growth can be investigated by combining the administration of AOM with the inflamma…

Colorectal cancerAzoxymethaneInflammationDiseaseTumor initiationBiologyBioinformaticsGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundMiceIn vivomedicineAnimalsCarcinogenAzoxymethaneDextran Sulfatemedicine.diseaseDisease Models AnimalchemistryTumor progressionColonic NeoplasmsCancer researchCarcinogensDisease Progressionmedicine.symptomInflammation MediatorsMutagensNature protocols
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Mode of interaction of different polyanions with the first (), the second (C2) and the fourth (C4) component of complement—II

1976

Abstract Dextran sulfate, polyvinyl sulfate, liquoid, heparin and Sp 54, ∗ (a pentosanpoly-sulfoester) prevented the uptake of C2 by EAC4b. In contrast to EAC 4 b 2 a , treatment of EAC4b2 with polyanions led to dissociation into EAC4b and C2. The inhibition of C2 uptake by polyanions could be reduced by increasing magnesium concentration to levels which are normally inhibitory, suggesting that Mg ++ ions are sequestered by these sulfated polyanions.

Complement component 2StereochemistryChemistryMagnesiumRehabilitationtechnology industry and agriculturechemistry.chemical_elementPhysical Therapy Sports Therapy and Rehabilitationmacromolecular substancesGeneral MedicineHeparinMedicinal chemistryDissociation (chemistry)SulfationDextran sulfatePolyvinyl sulfatemedicinemedicine.drugImmunochemistry
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Digestive vacuole of Plasmodium falciparum released during erythrocyte rupture dually activates complement and coagulation.

2012

Abstract Severe Plasmodium falciparum malaria evolves through the interplay among capillary sequestration of parasitized erythrocytes, deregulated inflammatory responses, and hemostasis dysfunction. After rupture, each parasitized erythrocyte releases not only infective merozoites, but also the digestive vacuole (DV), a membrane-bounded organelle containing the malaria pigment hemozoin. In the present study, we report that the intact organelle, but not isolated hemozoin, dually activates the alternative complement and the intrinsic clotting pathway. Procoagulant activity is destroyed by phospholipase C treatment, indicating a critical role of phospholipid head groups exposed at the DV surfa…

HemeproteinsMalePain ThresholdErythrocytesImmunologyComplement Pathway AlternativePlasmodium falciparumVacuoleBiochemistryHemolysisMonocytesMicrobiologyHypesthesiaRats Sprague-DawleyPhagocytosisparasitic diseasesAnimalsHumansMalaria FalciparumBlood CoagulationLungbiologyPhospholipase CHemozoinDextran SulfatePlasmodium falciparumCell BiologyHematologyIntracellular Membranesbiology.organism_classificationComplement systemRatsAntibody opsonizationImmunologyVacuolesAlternative complement pathwaySpleenWaste disposalBlood
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Effects of Dextran Sulfate 500 on Cell-Mediated Resistance to Infection with Listeria monocytogenes in Mice.

1974

Injection of dextran sulfate 500 caused loss of antibacterial resistance. Mice became more susceptible to an infection with Listeria monocytogenes and were unable to develop antilisterial immunity after both active and passive immunization with passively administered spleen cells from Listeria -immune donors. Indirect evidence suggests that the phagocytic component of cell-mediated resistance to bacterial infection is the site of attack of dextran sulfate.

ImmunologySpleenBiologybiochemical phenomena metabolism and nutritionmedicine.disease_causeMicrobiologyCell mediated immunityMicrobiologyIndirect evidenceInfectious Diseasesmedicine.anatomical_structureDextran sulfateImmunizationAntibacterial resistanceListeria monocytogenesImmunitymedicineParasitologyInfection and immunity
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Morphological Changes Induced by Dextran Sulfate 500 in Mononuclear Phagocytes of Listeria-Infected Mice

1974

Morphological changes involving mononuclear phagocytes in Listeria -infected mice after treatment with dextran sulfate 500 were investigated. Mononuclear phagocytes in livers and spleens, both circulating monocytes and fixed macrophages, showed uptake of electron-dense material. Mononuclear phagocyte changes were most pronounced within granulomatous lesions, where many phagocytes showed large membrane-bound inclusions and extensive cellular damage. It is concluded that dextran sulfate 500 selectively damages mononuclear phagocytes and that, in listerial infection, dextran sulfate 500 renders mononuclear phagocytes unable to express cellular resistance.

Infectious DiseasesDextran sulfateImmunologyImmunologyListeriaParasitologyMononuclear phagocyte systemBiologybiology.organism_classificationMicrobiologyGranulomatous lesionsAfter treatmentMicrobiology
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Leptin: A pivotal mediator of intestinal inflammation in mice

2002

Abstract Background & Aims: In addition to acting as a regulator of food intake and energy expenditure, leptin can also modulate immune and inflammatory responses. The role of leptin in intestinal inflammation is the focus of the present study. Methods: Acute and chronic colitis were induced in leptin-deficient ob/ob or wild-type (WT) mice using dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS). The severity of colitis was evaluated, and possible mechanisms were studied. Results: Leptin directly stimulates intraepithelial lymphocytes (IELs) and lamina propria mononuclear cells (LPMCs). In the DSS acute model, ob/ob mice exhibited a 72% reduction of colitis severity and sp…

LeptinSTAT3 Transcription Factormedicine.medical_specialtyColonanimal diseasesdigestive systemMonocytesProinflammatory cytokineMiceReference ValuesInternal medicinemedicineAnimalsInterferon gammaLymphocytesObesityIntestinal MucosaColitisMacrophage inflammatory proteinCells CulturedLeptin DeficiencyHepatologybusiness.industryLeptinDextran SulfateGastroenterologyColitismedicine.diseasedigestive system diseasesDNA-Binding ProteinsIsoenzymesMice Inbred C57BLEndocrinologyTrinitrobenzenesulfonic AcidCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesEnzyme InductionChronic DiseaseImmunologyTrans-ActivatorsCytokinesIntraepithelial lymphocyteFemaleTumor necrosis factor alphaDisease SusceptibilityChemokinesbusinessmedicine.drugGastroenterology
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