Search results for "tumor necrosis factor-alpha"

showing 10 items of 504 documents

A novel rat model of chronic fibrosing cholangitis induced by local administration of a hapten reagent into the dilated bile duct is associated with …

2000

Abstract Background/Aim: The cholangiopathies represent hepatobiliary diseases in which bile-duct epithelial cells are targets for destructive processes, including immune-mediated damage. We describe a novel rat model of chronic fibrosing cholangitis induced by administration of the hapten reagent 2,4,6-trinitrobenzenesulfonic acid (TNBS) into the dilated bile duct. Methods: The common bile duct was dilated due to a mild stenosis in 8-week-old female Lewis rats. TNBS (50 mg/kg) was injected during a second laparotomy. Results: TNBS-treatment reproducibly resulted in chronic fibrosing cholangitis. In retrograde cholangiography the bile ducts showed irregularities, beading and strictures. Alk…

MalePathologymedicine.medical_specialtyCholangitis SclerosingInflammatory bowel diseasePrimary sclerosing cholangitisAntibodies Antineutrophil CytoplasmicInjectionsEpitopesInterferon-gammaCholangiographyMedicineAnimalsChronic CholangitisRats Inbred BUFAutoantibodiesHepatologybiologymedicine.diagnostic_testCommon bile ductbusiness.industryTumor Necrosis Factor-alphamedicine.diseaseInterleukin-10Ratsmedicine.anatomical_structureLiverTrinitrobenzenesulfonic AcidRats Inbred LewMyeloperoxidaseChronic Diseasebiology.proteinAlkaline phosphataseTumor necrosis factor alphaFemaleBile DuctsbusinessCholangiographyJournal of hepatology
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The effect of the pro-inflammatory cytokine tumor necrosis factor-alpha on human joint capsule myofibroblasts.

2009

Introduction Previous studies have shown that the number of myoblastically differentiated fibroblasts known as myofibroblasts (MFs) is significantly increased in stiff joint capsules, indicating their crucial role in the pathogenesis of post-traumatic joint stiffness. Although the mode of MFs' function has been well defined for different diseases associated with tissue fibrosis, the underlying mechanisms of their regulation in the pathogenesis of post-traumatic joint capsule contracture are largely unknown. Methods In this study, we examined the impact of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α) on cellular functions of human joint capsule MFs. MFs were challenged w…

MalePathologymedicine.medical_treatmentFluorescent Antibody TechniqueGene ExpressionDinoprostExtracellular matrixPathogenesisElbow JointImmunology and AllergyCells CulturedReverse Transcriptase Polymerase Chain ReactionAntibodies MonoclonalMiddle AgedImmunohistochemistryExtracellular MatrixCytokinemedicine.anatomical_structureAntirheumatic AgentsCytokinesTumor necrosis factor alphaFemaleHip Jointmedicine.symptomInflammation MediatorsMyofibroblastmusculoskeletal diseasesmedicine.medical_specialtyanimal structuresContractureDiclofenacImmunologyBlotting Westernmacromolecular substancesBiologyCollagen Type IDinoprostoneRheumatologyJoint capsuleResearch articlemedicineHumansAgedCell ProliferationCyclooxygenase 2 InhibitorsTumor Necrosis Factor-alphaProstaglandins FFibroblastsActinsInfliximabCyclooxygenase 2Joint stiffnessContractureJoint CapsuleArthritis researchtherapy
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Glutamine potentiates TNF-α-induced tumor cytotoxicity

2001

L-glutamine (Gln) sensitizes tumor cells to tumor necrosis factor (TNF)-alpha-induced cytotoxicity. The type and mechanism of cell death induced by TNF-alpha was studied in Ehrlich ascites tumor (EAT)-bearing mice fed a Gln-enriched diet (GED; where 30% of the total dietary nitrogen was from Gln). A high rate of Gln oxidation promotes a selective depletion of mitochondrial glutathione (mtGSH) content to approximately 58% of the level found in tumor mitochondria of mice fed a nutritionally complete elemental diet (standard diet, SD). The mechanism of mtGSH depletion involves a glutamate-induced inhibition of GSH transport from the cytosol into mitochondria. The increase in reactive oxygen in…

MaleProgrammed cell deathFree RadicalsCell SurvivalGlutamineApoptosisCytochrome c GroupMitochondrionBiologyBiochemistryMembrane PotentialsMiceNecrosischemistry.chemical_compoundAdenosine TriphosphateSuperoxidesPhysiology (medical)Tumor Cells CulturedAnimalsButhionine sulfoximineCaspase 3Tumor Necrosis Factor-alphaDrug SynergismHydrogen PeroxideGlutathioneGlutathioneMolecular biologyDietMitochondriaCell biologyOxygenGlutamineOxidative StressCytosolProto-Oncogene Proteins c-bcl-2chemistryApoptosisCaspasesReactive Oxygen SpeciesOxidation-ReductionCell DivisionIntracellularFree Radical Biology and Medicine
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Bcl-2 and Mn-SOD antisense oligodeoxynucleotides and a glutamine-enriched diet facilitate elimination of highly resistant B16 melanoma cells by tumor…

2005

Mitochondrial glutathione (mtGSH) depletion increases sensitivity of Bcl-2-overexpressing B16 melanoma (B16M)-F10 cells (high metastatic potential) to tumor necrosis factor-alpha (TNF-alpha)-induced oxidative stress and death in vitro. In vivo, mtGSH depletion in B16M-F10 cells was achieved by feeding mice (where the B16M-F10 grew as a solid tumor in the footpad) with an L-glutamine (L-Gln)-enriched diet, which promoted in the tumor cells an increase in glutaminase activity, accumulation of cytosolic L-glutamate, and competitive inhibition of GSH transport into mitochondria. L-Gln-adapted B16M-F10 cells, isolated using anti-Met-72 monoclonal antibodies and flow cytometry-coupled cell sortin…

MaleProgrammed cell deathgovernment.form_of_governmentGlutamineSOD2Antineoplastic AgentsSoft Tissue NeoplasmsMitochondrionBiologyBiochemistryGlutaminase activitySuperoxide dismutaseMiceAnimalsMolecular BiologyMelanomaAntisense therapySuperoxide DismutaseTumor Necrosis Factor-alphaCell BiologyGenetic TherapyOligonucleotides AntisenseMolecular biologyAnimal FeedCombined Modality TherapyGlutathioneMitochondriaMice Inbred C57BLDisease Models AnimalOxidative StressMitochondrial permeability transition poreProto-Oncogene Proteins c-bcl-2Drug Resistance Neoplasmgovernmentbiology.proteinTumor necrosis factor alphaNeoplasm TransplantationThe Journal of biological chemistry
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Exercise promotes IL-6 release from legs in older men with minor response to unilateral immobilization

2015

Physical inactivity is a major contributor to low-grade systemic inflammation. Most of the studies characterizing interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) release from exercising legs have been done in young, healthy men, but studies on inactivity in older people are lacking. The impact of 14 days of one-leg immobilization (IM) on IL-6 and TNF-α release during exercise in comparison to the contralateral control (CON) leg was investigated. Fifteen healthy men (age 68.1 ± 1.1 year (mean ± SEM); BMI 27.0 ± 0.4 kg·m(2); VO2max 33.3 ± 1.6 ml·kg(‒1)·min(‒1)) performed 45 min of two-leg dynamic knee extensor exercise at 19.5 ± 0.9 W. Arterial and femoral venous blood samples from …

MaleRestraint Physical0301 basic medicinemedicine.medical_specialtyNecrosisPhysical Therapy Sports Therapy and RehabilitationThighSystemic inflammationCohort Studies03 medical and health sciences0302 clinical medicineHumansMedicineOrthopedics and Sports MedicineInterleukin 6ExerciseAgedLegKnee extensorsbiologyInterleukin-6Tumor Necrosis Factor-alphabusiness.industryGeneral MedicineVenous bloodBlood flowSurgery030104 developmental biologymedicine.anatomical_structureAnesthesiabiology.proteinmedicine.symptombusiness030217 neurology & neurosurgeryMinor ResponseEuropean Journal of Sport Science
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Subclinical atherosclerosis and fetuin-A plasma levels in essential hypertensive patients

2012

The intima-media thickness (IMT) is considered as a surrogate marker for atherosclerotic disease. The aim of this study was to analyze the relationship of carotid IMT with fetuin-A in patients with essential hypertension (EH) and normal renal function. The plasma levels of fetuin-A, interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and the biomarker of oxidative stress 8-iso-PGF2alpha were assayed in samples from 105 untreated EH patients. Carotid IMT measurements were also performed. EH was studied overall and after dividing in EH with IMT ≥ and 0.9 mm (AUC (area under the curve) 0.738, P<0.0001). Our results suggest that in EH, fetuin-A is associated with the IMT independently of oxid…

MaleSettore MED/09 - Medicina Internaalpha-2-HS-GlycoproteinPhysiologyDinoprostKidneyEssential hypertensionmedicine.disease_causeCarotid Intima-Media ThicknessGastroenterologyatherosclerosiRisk FactorsMedicinebiologyArea under the curveMiddle Agedmusculoskeletal systemHypertensioncardiovascular systemRegression AnalysisBiomarker (medicine)FemaleEssential HypertensionCardiology and Cardiovascular MedicineAdultmedicine.medical_specialtyRenal functionPredictive Value of TestsInternal medicineInternal MedicineHumanscardiovascular diseasesintima-media thicknessInterleukin 6Settore MED/14 - NefrologiaInterleukin-6Tumor Necrosis Factor-alphabusiness.industrySurrogate endpointAtherosclerosismedicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareFetuinfetuin-AOxidative StressCross-Sectional StudiesEndocrinologyinflammationCase-Control Studiesbiology.proteinbusinessBiomarkersOxidative stressHypertension Research
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Obesity and reduction of the response rate to anti-tumor necrosis factor α in rheumatoid arthritis: an approach to a personalized medicine.

2013

Objective Obesity is a mild, long-lasting inflammatory disease and, as such, could increase the inflammatory burden of rheumatoid arthritis (RA). The study aim was to determine whether obesity represents a risk factor for a poor remission rate in RA patients requiring anti–tumor necrosis factor α (anti-TNFα) therapy for progressive and active disease despite treatment with methotrexate or other disease-modifying antirheumatic drugs. Methods Patients were identified from 15 outpatient clinics of university hospitals and hospitals in Italy taking part in the Gruppo Italiano di Studio sulle Early Arthritis network. Disease Activity Score in 28 joints (DAS28), body mass index (BMI; categorized …

MaleSettore MED/16 - REUMATOLOGIAArthritisGastroenterologyReceptors Tumor Necrosis FactorEtanerceptEtanerceptArthritis RheumatoidRheumatoidMonoclonalReceptorsMedicineOutpatient clinicLongitudinal StudiesRegistriesPrecision Medicineskin and connective tissue diseasesHumanizedRemission InductionAntibodies MonoclonalIndividualized MedicineMiddle AgedTreatment OutcomeRheumatoid arthritisAntirheumatic AgentsFemaleDrugmedicine.drugmusculoskeletal diseasesmedicine.medical_specialtyAdalimumab; Aged; Antibodies Monoclonal; Antibodies Monoclonal Humanized; Antirheumatic Agents; Arthritis Rheumatoid; Dose-Response Relationship Drug; Etanercept; Female; Humans; Immunoglobulin G; Infliximab; Longitudinal Studies; Male; Middle Aged; Obesity; Precision Medicine; Receptors Tumor Necrosis Factor; Registries; Remission Induction; Treatment Outcome; Tumor Necrosis Factor-alphaAntibodies Monoclonal HumanizedAntibodiesDose-Response RelationshipRheumatologyInternal medicineAdalimumabHumansObesityRisk factorAgedDose-Response Relationship Drugbusiness.industryTumor Necrosis Factor-alphaArthritisAdalimumabmedicine.diseaseInfliximabRheumatologyInfliximabAged; Antibodies Monoclonal; Antibodies Monoclonal Humanized; Antirheumatic Agents; Arthritis Rheumatoid; Dose-Response Relationship Drug; Female; Humans; Immunoglobulin G; Individualized Medicine; Longitudinal Studies; Male; Middle Aged; Obesity; Receptors Tumor Necrosis Factor; Registries; Remission Induction; Treatment Outcome; Tumor Necrosis Factor-alphaImmunoglobulin GImmunologybusinessTumor Necrosis FactorArthritis careresearch
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Activation of the Constitutive Androstane Receptor Inhibits Leukocyte Adhesiveness to Dysfunctional Endothelium

2021

Leukocyte cell recruitment into the vascular subendothelium constitutes an early event in the atherogenic process. As the effect of the constitutive androstane receptor (CAR) on leukocyte recruitment and endothelial dysfunction is poorly understood, this study investigated whether the role of CAR activation can affect this response and the underlying mechanisms involved. Under physiological flow conditions, TNFα-induced endothelial adhesion of human leukocyte cells was concentration-dependently inhibited by preincubation of human umbilical arterial endothelial cells with the selective human CAR ligand CITCO. CAR agonism also prevented TNFα induced VCAM-1 expression, as well as MCP-1/CCL-2 a…

MaleSmall interfering RNAEndotheliumQH301-705.5Receptors Cytoplasmic and NuclearVascular Cell Adhesion Molecule-1Leukocyte RollingRetinoid X receptorArticleendothelial dysfunctionCatalysisInorganic ChemistryMiceConstitutive androstane receptorCell AdhesionHuman Umbilical Vein Endothelial CellsLeukocytesmedicineAnimalsHumansBiology (General)Physical and Theoretical ChemistryEndothelial dysfunctionQD1-999Molecular BiologySpectroscopyconstitutive androstane receptorTumor Necrosis Factor-alphaChemistryOrganic ChemistryNF-kappa BEndothelial Cellsleukocyte recruitmentGeneral Medicinemedicine.diseaseComputer Science ApplicationsCell biologyChemistrymedicine.anatomical_structureGene Expression RegulationTumor necrosis factor alphaIntravital microscopySignal TransductionInternational Journal of Molecular Sciences
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Immuno-inflammatory activation in acute cardio-embolic strokes in comparison with other subtypes of ischaemic stroke

2009

Few studies have examined the relationship between inflammatory biomarker blood levels, cardioembolic stroke subtype and neurological deficit. So the aim of our study is to evaluate plasma levels of immuno-inflammatory variables in patients with cardio-embolic acute ischaemic stroke compared to other diagnostic subtypes and to evaluate the relationship between immuno-inflammatory variables, acute neurological deficit and brain infarct volume. One hundred twenty patients with acute ischaemic stroke and 123 controls without a diagnosis of acute ischaemic stroke were evaluated. The type of acute ischaemic stroke was classified according to the TOAST classification. We evaluated plasma levels o…

MaleTOAST Classificationmedicine.medical_specialtySettore MED/09 - Medicina InternaHeart DiseasesEmbolismInterleukin-1betaSeverity of Illness IndexBrain Ischemiacytokines stroke cardioembolicCentral nervous system diseaseBrain ischemiaDisability EvaluationPredictive Value of TestsInternal medicineSeverity of illnessmedicineHumanscardiovascular diseasesStrokeAgedAged 80 and overInterleukin-6Tumor Necrosis Factor-alphaVascular diseasebusiness.industryCerebral infarctionCase-control studyHematologyMiddle Agedmedicine.diseaseSurgeryStrokeRisk Factors inflammation cytokines Stroke Cerebral infarct cerebrovascular disease cerebrovascular accidentCase-Control StudiesLinear ModelsCardiologyFemaleSettore MED/26 - NeurologiaInflammation MediatorsbusinessBiomarkers
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Pancreatic ascites hemoglobin contributes to the systemic response in acute pancreatitis.

2015

Upon hemolysis extracellular hemoglobin causes oxidative stress and cytotoxicity due to its peroxidase activity. Extracellular hemoglobin may release free hemin, which increases vascular permeability, leukocyte recruitment, and adhesion molecule expression. Pancreatitis-associated ascitic fluid is reddish and may contain extracellular hemoglobin. Our aim has been to determine the role of extracellular hemoglobin in the local and systemic inflammatory response during severe acute pancreatitis in rats. To this end we studied taurocholate-induced necrotizing pancreatitis in rats. First, extracellular hemoglobin in ascites and plasma was quantified and the hemolytic action of ascitic fluid was …

MaleTaurocholic AcidVascular Endothelial Growth Factor Amedicine.medical_specialtyNecrosisInterleukin-1betaAbdominal FatAdipose tissueVascular permeabilityInflammationBiochemistryHemoglobinsNecrosisPhysiology (medical)Internal medicinemedicineExtracellularAnimalsAscitic FluidPeritoneal LavageRats WistarPancreasPeroxidasebusiness.industryPancreatitis Acute NecrotizingTumor Necrosis Factor-alphaAscitesmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitInterleukin-10RatsOxidative StressEndocrinologyGene Expression RegulationImmunologyPancreatitisAcute pancreatitisHemoglobinmedicine.symptombusinessFree radical biologymedicine
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