Search results for "tumor necrosis factor-alpha"

showing 10 items of 504 documents

Search for genetic factors associated with susceptibility to multiple sclerosis.

2006

Multiple sclerosis (MS) is a cell-mediated autoimmune disease characterized by type-1 cytokine production. Environmental and individual genetic background might influence this response particularly in cytokine gene polymorphisms. We evaluated whether polymorphisms of interleukin (IL)-10, IL-12, and tumor necrosis factor (TNF)-alpha genes, which might play a role in MS pathogenesis, are associated with MS susceptibility. Genotype frequencies for all the analyzed polymorphisms were not differently distributed between cases and controls. It is reasonable to suppose that the cytokine single-nucleotide polymorphisms (SNPs) studied must be considered against a larger genetic background involving …

MaleMultiple Sclerosismedicine.medical_treatmentSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceGene FrequencymedicineSNPHumansGenetic Predisposition to DiseaseGeneticsAutoimmune diseasePolymorphism GeneticTumor Necrosis Factor-alphaGeneral NeuroscienceMultiple sclerosisInterleukinmedicine.diseaseInterleukin-12Genotype frequencyInterleukin-10tumor necrosis factor alpha genetic polymorphism genetic susceptibility genotype heredity human major clinical studyInterleukin 10CytokineCase-Control StudiesImmunologyCytokinesFemaleDisease SusceptibilityAnnals of the New York Academy of Sciences
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Interferon-γ Induces Chronic Active Myocarditis and Cardiomyopathy in Transgenic Mice

2007

Chronic heart failure is associated with an activation of the immune system characterized among other factors by the cardiac synthesis and serum expression of proinflammatory cytokines. There is unequivocal clinical and experimental evidence that the cytokine tumor necrosis factor-alpha is involved in the development of chronic heart failure, but a putative cardiotoxic potential of the proinflammatory cytokine interferon (IFN)-gamma remains primarily unknown. To investigate this issue we analyzed the cardiac phenotype of SAP-IFN-gamma transgenic mice, which constitutively express IFN-gamma in their livers and hence exhibit high circulating serum levels of this cytokine. SAP-IFN-gamma mice s…

MaleMyocarditismedicine.medical_treatmentT-LymphocytesCardiomyopathyGene ExpressionMice Inbred StrainsMice Transgenic030204 cardiovascular system & hematologyBiologyPathology and Forensic MedicineProinflammatory cytokine03 medical and health sciencesInterferon-gammaMice0302 clinical medicinemedicineAnimalsHumansInterferon gammaIntestinal MucosaPromoter Regions Genetic030304 developmental biology0303 health sciencesCardiotoxicityReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaMacrophagesHeartDendritic Cellsmedicine.diseaseInterleukin-123. Good healthRatsIntestinesMice Inbred C57BLMyocarditisSerum Amyloid P-ComponentCytokineEchocardiographyImmunologyChronic DiseaseInterleukin 12Tumor necrosis factor alphaFemaleCardiomyopathiesmedicine.drugRegular Articles
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Glutathione and the rate of cellular proliferation determine tumour cell sensitivity to tumour necrosis factor in vivo.

1997

Low rates of cellular proliferation are associated with low GSH content and enhanced sensitivity of Ehrlich ascites-tumour (EAT) cells to the cytotoxic effects of recombinant human tumour necrosis factor (rhTNF-alpha). Buthionine sulphoximine, a selective inhibitor of GSH synthesis, inhibited tumour growth and increased rhTNF-alpha cytoxicity in vitro. Administration of sublethal doses (10(6)units/kg per day) of rhTNF-alpha to EAT-bearing mice promoted oxidative stress (as measured by increases in intracellular peroxide levels, O2(-); generation and mitochondrial GSSG) and resulted in a slight reduction (19%) in tumour cell number when controls showed the highest rate of cellular proliferat…

MaleNecrosisCell SurvivalMice Inbred StrainsBiologyPharmacologymedicine.disease_causeBiochemistrychemistry.chemical_compoundMiceIn vivomedicineTumor Cells CulturedCytotoxic T cellAnimalsHumansCytotoxicityCarcinoma Ehrlich TumorMolecular BiologyButhionine SulfoximineTumor Necrosis Factor-alphaDrug SynergismCell BiologyGlutathioneGlutathioneRecombinant ProteinsKineticschemistryBiochemistryCancer cellmedicine.symptomOxidative stressIntracellularCell DivisionResearch ArticleThe Biochemical journal
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Suppression of leukotriene B4 and tumour necrosis factor alpha release in acute inflammatory responses by novel prenylated hydroquinone derivatives.

1998

A series of prenyl hydroquinone derivatives synthesized as structural analogs of marine products were tested for their effects on inflammatory responses in vitro and in vivo. 2-Prenyl-1,4-hydroquinone (H1), 2-diprenyl-1,4-hydroquinone (H2), 2-triprenyl-1,4-hydroquinone (H3) and 2-tetraprenyl-1,4-hydroquinone (H4) scavenged reactive oxygen species and inhibited 5-lipoxygenase (5-LO) activity in human neutrophils. The inhibition of 5-LO activity was demonstrated in vivo in the mouse air pouch injected with zymosan and arachidonic acid-induced ear inflammation. The four compounds suppressed the production of tumour necrosis factor alpha (TNFalpha) in J774 cells stimulated with lipopolysacchari…

MaleNecrosisLipopolysaccharideLeukotriene B4Anti-Inflammatory AgentsPharmacologyLeukotriene B4Dinoprostonechemistry.chemical_compoundMiceIn vivomedicineAnimalsEdemaHumansCells CulturedNitritesPharmacologyInflammationArachidonic AcidbiologyTumor Necrosis Factor-alphaZymosanGeneral MedicineHydroquinonesNitric oxide synthasechemistryBiochemistryDepression ChemicalArachidonate 5-lipoxygenaseLuminescent Measurementsbiology.proteinTumor necrosis factor alphamedicine.symptomNaunyn-Schmiedeberg's archives of pharmacology
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Leishmaniasis, autoimmune rheumatic disease, and anti–tumor necrosis factor therapy, Europe.

2009

We report 2 cases of leishmaniasis in patients with autoimmune rheumatic diseases in Greece. To assess trends in leishmaniasis reporting in this patient population, we searched the literature for similar reports from Europe. Reports increased during 2004–2008, especially for patients treated with anti–tumor necrosis factor agents.

MaleNecrosisgenetic structuresEpidemiologymedicine.medical_treatmentAnti-Inflammatory Agentslcsh:MedicineAnti-TNF0302 clinical medicineRisk FactorsMedicine030212 general & internal medicinerheumatic diseaseLeishmaniasisLeishmaniaimmunosuppressionbiologyDispatchAntibodies MonoclonalRheumatic diseaseImmunosuppressionMiddle Aged3. Good healthEuropeTreatment OutcomeInfectious DiseasesRheumatic feverFemaleTumor necrosis factor alphaImmunotherapymedicine.symptomMicrobiology (medical)medicine.medical_specialtytumor necrosis factor030231 tropical medicineletterparasiteslcsh:Infectious and parasitic diseases03 medical and health sciencesRheumatic DiseasesAnimalsHumansautoimmune diseaseslcsh:RC109-216Letters to the EditorAged030203 arthritis & rheumatologyTumor Necrosis Factor-alphabusiness.industryscreeninglcsh:RLeishmaniasisImmunotherapyLeishmaniabiology.organism_classificationmedicine.diseaseDermatologyInfliximabAnti-Tumor Necrosis Factor TherapyImmunologysense organsbusinessEmerging Infectious Diseases
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Effect of sulfur dioxide on cytokine production of human alveolar macrophages in vitro.

1996

Tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and transforming growth factor-beta are cytokines synthesized by alveolar macrophages. We investigated the effect of sulfur dioxide, a major air pollutant, on the production of these cytokines by alveolar macrophages. The cells were layered on a polycarbonate membrane and exposed for 30 min to 0.0, 1.0, 2.5, and 5.0 ppm sulfur dioxide at 37 degrees C and 100% air humidity. The cells were incubated for 24 h after exposure, thus allowing cytokine release. Cytotoxic effects of sulfur dioxide were evaluated by trypan blue exclusion. Cytokines were measured with enzyme-linked immunosorbent assays (i.e., tumor necrosis factor-alpha, i…

MaleNecrosismedicine.medical_treatmentEnzyme-Linked Immunosorbent Assaychemistry.chemical_compoundTransforming Growth Factor betaMacrophages AlveolarmedicineEnvironmental ChemistryMacrophageHumansSulfur DioxideSulfur dioxideCells CulturedGeneral Environmental ScienceAir PollutantsDose-Response Relationship DrugChemistryTumor Necrosis Factor-alphaInterleukinsPublic Health Environmental and Occupational HealthMiddle AgedMolecular biologymedicine.anatomical_structureCytokineImmunologyToxicityTrypan blueTumor necrosis factor alphaFemalemedicine.symptomPulmonary alveolusArchives of environmental health
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Toll-like receptor 4 defective mice carrying point or null mutations do not show increased susceptibility toCandida albicansin a model of hematogenou…

2006

We have studied the role of TLR4 in murine defenses against Candida albicans in two TLR4-defective mouse strains: C3H/HeJ mice which have defective TLR4 signaling, and TLR4-/- knockout mice. Both TLR4-defective mice strains experimentally infected with virulent C. albicans cells showed no significant difference in survival as compared with their respective controls. Recruitment of neutrophils to the peritoneal cavity of i.p. infected mice was not affected in TLR4-/-animals, but significantly enhanced in C3H/HeJ mice, compared with their control mice. In vitro production of TNF-alpha by macrophages from both types of TLR4-defective mice, in response to yeasts and hyphae of C. albicans, was n…

MaleNeutrophilsBiologyMicrobiologyInterferon-gammaMicePeritoneal cavityCandida albicansSplenocytemedicineAnimalsPoint MutationGenetic Predisposition to DiseaseCandida albicansMice KnockoutMice Inbred C3HToll-like receptorTumor Necrosis Factor-alphaCandidiasisGeneral MedicineTh1 CellsFlow Cytometrybiology.organism_classificationInterleukin-12Corpus albicansMice Inbred C57BLToll-Like Receptor 4Infectious Diseasesmedicine.anatomical_structureKnockout mouseMacrophages PeritonealTLR4Femalelipids (amino acids peptides and proteins)Tumor necrosis factor alphaMedical Mycology
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Influence of Age on Brain Edema Formation, Secondary Brain Damage and Inflammatory Response after Brain Trauma in Mice

2012

After traumatic brain injury (TBI) elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, neuroinflammation and secondary brain damage after brain trauma in mice. Young (2 months) and old (21 months) male C57Bl6N mice were anesthetized and subjected to a controlled cortical impact injury (CCI) on the right parietal cortex. Animals of both ages were randomly assigned to 15 min, 24 h, and 72 h survival. At the end of the observation periods, contusion volume, brain water content, neurolo…

MalePathologyAgingAnatomy and PhysiologyCritical Care and Emergency MedicineMouseT-LymphocytesInterleukin-1beta610 MedizinNitric Oxide Synthase Type IISystemic inflammationMiceAnesthesiologyCell Movement610 Medical sciencesEdemaImmune PhysiologyEdemaLungNeurosurgical CareMultidisciplinaryHematologic TestsQRAging and ImmunityAnimal ModelsOrgan SizeHead Injurymedicine.anatomical_structureNeurologyNeurointensive CareCytokinesMedicinemedicine.symptomResearch Articlemedicine.medical_specialtyTraumatic brain injuryScienceImmunologyInflammationBrain damageAtrophyModel OrganismsNeurorehabilitation and TraumamedicineAnimalsRNA MessengerBiologyCerebrumNeuroinflammationInflammationLungbusiness.industryInterleukin-6Tumor Necrosis Factor-alphaImmunityWatermedicine.diseaseMice Inbred C57BLGene Expression RegulationCyclooxygenase 2Immune SystemBrain InjuriesClinical ImmunologybusinessPhysiological ProcessesPLoS ONE
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Expression of Interleukin-32 in the Inflamed Arteries of Patients With Giant Cell Arteritis

2011

Objective Giant cell (temporal) arteritis (GCA) is a vasculitis that mainly affects the large and medium arteries, especially the branches of the proximal aorta. Interleukin-32 (IL-32) is a recently described Th1 proinflammatory cytokine, and is mainly induced by interferon-γ (IFNγ), IL-1β, and tumor necrosis factor α (TNFα). This study was undertaken to investigate the expression and tissue distribution of IL-32 in artery biopsy specimens from patients with GCA. Methods Quantitative gene expression analysis of IL-32, IL-1β, TNFα, IFNγ, IL-6, and IL-27 was performed in artery biopsy specimens obtained from 18 patients with GCA and 15 controls. Immunohistochemistry analysis was performed to …

MalePathologyInterleukin-1betaMessenger80 and overImmunology and AllergyPharmacology (medical)Giant Cell ArteritiAged 80 and overeducation.field_of_studyReverse Transcriptase Polymerase Chain ReactionInterleukin-17StatisticsArteriesMiddle AgedFlow CytometryImmunohistochemistryTh1 responseFemaleInterleukin 17VasculitisInterleukin-32; Giant Cell Arteritis; Th1 responsemedicine.medical_specialtyGiant Cell ArteritisImmunologyPopulationBiologyStatistics NonparametricProinflammatory cytokineInterferon-gammaRheumatologymedicine.arterymedicineHumansNonparametricRNA MessengerArteritiseducationAgedAortaAged; Aged 80 and over; Arteries; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; Interferon-gamma; Interleukin-17; Interleukin-1beta; Interleukin-6; Interleukins; Male; Middle Aged; RNA Messenger; Reverse Transcriptase Polymerase Chain Reaction; Statistics Nonparametric; Th1 Cells; Tumor Necrosis Factor-alphaInterleukin-6Tumor Necrosis Factor-alphaInterleukinsTh1 Cellsmedicine.diseaseInterleukin-32Giant cell arteritisGiant cellImmunologyRNA
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Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
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