Search results for "tumor necrosis factor-alpha"

showing 10 items of 504 documents

Damping excessive inflammation and tissue damage in Mycobacterium tuberculosis infection by Toll IL-1 receptor 8/single Ig IL-1-related receptor, a n…

2007

Abstract Toll IL-1R 8/single Ig IL-1-related receptor (TIR8/SIGIRR) is a member of the IL-1R family, expressed by epithelial tissues and immature dendritic cells, and is regarded as a negative regulator of TLR/IL-1R signaling. Tir8-deficient mice were rapidly killed by intranasal administration of low doses of Mycobacterium tuberculosis, despite controlling efficiently the number of viable bacilli in different organs. Tir8−/−-infected mice showed an increased number of neutrophils and macrophages in the lungs; however, mycobacteria-specific CD4 and CD8 T cells were similar in Tir8−/− and Tir8+/+ mice. Exaggerated mortality of Tir8−/− mice was due to massive liver necrosis and was accompanie…

TuberculosisNeutrophilsImmunologyInterleukin-1betaInflammationBiologyPeripheral blood mononuclear cellAntibodiesMycobacterium tuberculosisMiceNecrosisCell MovementMacrophages AlveolarmedicineImmunology and AllergyCytotoxic T cellAnimalsReceptorLungTuberculosis PulmonaryInflammationLungTumor Necrosis Factor-alphaToll-Like ReceptorsReceptors Interleukin-1Dendritic CellsMycobacterium tuberculosismedicine.diseasebiology.organism_classificationIn vitroMice Mutant Strainsmedicine.anatomical_structureLiverImmunologyCytokinesmedicine.symptomToll IL-1 Receptor 8/Single Ig IL-1-Related Receptor Inlfammation Mycobacterium tuberculosisInterleukin-1Signal Transduction
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Possible Mechanisms for Tumour Cell Sensitivity to TNF-a and Potential Therapeutic Applications

2001

TNF is a macrophage / monocyte-derived cytokine with cytostatic and cytotoxic anti-tumour activity. TNF-alpha can cause haemorrhagic necrosis and regression of experimental tumours. Nevertheless, the TNF-alpha doses required to cure tumour-bearing mice lead to injury of normal tissues and, eventually, may cause a lethal shock syndrome. This toxicity implies severe limitations for the therapeutic use of TNF-a. Reactive oxygen intermediates (ROIs) are involved in TNF-a-induced cell killing. Different studies are consistent with the hypothesis that tumour cell sensitivity to TNF-alpha is related to its capacity to buffer oxidative attack. Recently, we have demonstrated that the sensitivity of …

Tumor Necrosis Factor-alphamedicine.medical_treatmentCellPharmaceutical ScienceGlutathionePharmacologyMitochondrionBiologychemistry.chemical_compoundCytokineCell killingmedicine.anatomical_structurechemistryBiochemistryDrug Resistance NeoplasmIn vivoNeoplasmsTumor Cells CulturedmedicineAnimalsHumansCytotoxic T cellTumor necrosis factor alphaBiotechnologyCurrent Pharmaceutical Biotechnology
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von Hippel-Lindau Protein-Mediated Repression of Tumor Necrosis Factor Alpha Translation Revealed through Use of cDNA Arrays

2003

Based on evidence that the von Hippel-Lindau (VHL) tumor suppressor protein is associated with polysomes and interacts with translation regulatory factors, we set out to investigate the potential influence of pVHL on protein translation. To this end, renal cell carcinoma (RCC) cells that either lacked pVHL or expressed pVHL through stable transfection were used to prepare RNA from cytosolic (unbound) and polysome-bound fractions. Hybridization of cDNA arrays using RNA from each fraction revealed a subset of transcripts whose abundance in polysomes decreased when pVHL function was restored. The tumor necrosis factor alpha (TNF-alpha) mRNA was identified as one of the transcripts that prefere…

Ubiquitin-Protein LigasesGene ExpressionEnzyme-Linked Immunosorbent AssayBiologyTransfectionurologic and male genital diseasesLigasesCytosolGenes ReporterPolysomeTumor Cells CulturedProtein biosynthesisHumansGenes Tumor SuppressorRNA Messenger3' Untranslated RegionsCarcinoma Renal CellMolecular BiologyOligonucleotide Array Sequence AnalysisReporter geneMessenger RNATumor Necrosis Factor-alphaThree prime untranslated regionGene Expression ProfilingTumor Suppressor ProteinsRNATranslation (biology)Cell BiologyTransfectionBlotting NorthernMolecular biologyfemale genital diseases and pregnancy complicationsGene Expression Regulation NeoplasticVon Hippel-Lindau Tumor Suppressor ProteinPolyribosomesProtein BiosynthesisMolecular and Cellular Biology
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Prostacyclin inhibits adhesion of polymorphonuclear leukocytes to human vascular endothelial cells due to adhesion molecule independent regulatory me…

2002

Prostacyclin is an important endothelial mediator involved in the interaction of neutrophils (PMN) with the vessel wall. Many studies have shown the beneficial effects of prostacyclin in ischemia and reperfusion. However, no previous study has investigated the direct effects of the prostacyclin analogs iloprost (ILO) and alprostadil (PGE(1)) on the endothelial part of the adhesion process. Human umbilical vein endothelial cells (HUVECs) were grown to confluence, stimulated with 300 U/ml TNF-alpha and treated with increasing concentrations of ILO and PGE(1). The cells were washed to remove TNF and the inhibitors and adhesion of fluorescence-green labeled PMN was determined microscopically. I…

Umbilical VeinsEndotheliumNeutrophilsPhysiologyVascular Cell Adhesion Molecule-1ProstacyclinPharmacologyUmbilical veinPhysiology (medical)Cell AdhesionmedicineHumansIloprostAlprostadilChemoattractant activityCells CulturedCell NucleusTumor Necrosis Factor-alphaChemistryChemotaxisAdhesionrespiratory systemEpoprostenolrespiratory tract diseasesEndothelial stem cellmedicine.anatomical_structureBiochemistrycardiovascular systemlipids (amino acids peptides and proteins)Tumor necrosis factor alphaEndothelium VascularCardiology and Cardiovascular MedicineCell Adhesion MoleculesIloprostmedicine.drugBasic Research in Cardiology
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Differential Effects of Biologics on Psoriasis-Related Vascular Inflammation and Risk of Thrombosis

2020

Programa Estatal de I+D+i Orientada a los Retos de la Sociedad from Ministerio de Ciencia, Innovación y Universidades and European Regional Development Fund (Spain) [RTI2018-094436-B-I00]; Ministerio de Sanidad y Consumo CIBERehd (Spain) [CB06/04/0071]; Generalitat Valenciana (Spain) [PROMETEO/2018/141]; Proyectos Grupos Emergentes [GV/2019/043]; and Universidad Europea (Spain) (2018/UEM32 and 2019/UEM29]. 8.551 JCR (2020) Q1, 4/69 Dermatology 1.951 SJR (2020) Q1, 54/438 Biochemistry No data IDR 2020 UEV

Vasculitis0301 basic medicinemedicine.medical_specialtyEnfermedad cardiovascularImiquimodCell CommunicationDermatologyBiochemistryMiceTrombosis03 medical and health sciences0302 clinical medicinePsoriasis Area and Severity IndexPsoriasisProductos biológicosLeukocytesmedicineAnimalsHumansPsoriasisMolecular BiologyBody surface areaBiological ProductsImiquimodTumor Necrosis Factor-alphabusiness.industryEndothelial CellsThrombosisCell BiologyDermatology Life Quality Indexmedicine.diseaseDermatologyThrombosis030104 developmental biology030220 oncology & carcinogenesisMethotrexatebusinessEnfermedad de la pielMacemedicine.drugJournal of Investigative Dermatology
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Replication of Human Norovirus in Mice after Antibiotic-Mediated Intestinal Bacteria Depletion

2022

Human noroviruses (HuNoVs) are the main cause of acute gastroenteritis causing more than 50,000 deaths per year. Recent evidence shows that the gut microbiota plays a key role in enteric virus infectivity. In this context, we tested whether microbiota depletion or microbiota replacement with that of human individuals susceptible to HuNoVs infection could favor viral replication in mice. Four groups of mice (n = 5) were used, including a control group and three groups that were treated with antibiotics to eliminate the autochthonous intestinal microbiota. Two of the antibiotic-treated groups received fecal microbiota transplantation from a pool of feces from infants (age 1-3 months) or an au…

Virus RNAMicrobiologiaAntibiòticsDNA RibosomalCatalysisInorganic ChemistryFecesMicenorovirus; antibiotic; microbiota; mice; virus sheddingAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologySpectroscopyCaliciviridae InfectionsInterleukin-13BacteriaTumor Necrosis Factor-alphaMicrobiotaNorovirusOrganic ChemistryAntibioticInfantVirus sheddingGeneral MedicineToll-Like Receptor 2Anti-Bacterial AgentsComputer Science ApplicationsInterleukin-4
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Vitamin A deficiency alters rat lung alveolar basement membrane: reversibility by retinoic acid.

2010

Vitamin A is essential for lung development and pulmonary cell differentiation and its deficiency results in alterations of lung structure and function. Basement membranes (BMs) are also involved in those processes, and retinoic acid, the main biologically active form of vitamin A, influences the expression of extracellular matrix macromolecules. Therefore, we have analyzed the ultrastructure and collagen content of lung alveolar BM in growing rats deficient in vitamin A and the recovering effect of all-trans retinoic acid. Male weanling pups were fed a retinol-adequate or -deficient diet until they were 60 days old. A group of vitamin A-deficient pups were recovered by daily intraperitonea…

VitaminCollagen Type IVMalemedicine.medical_specialtymedicine.drug_classEndocrinology Diabetes and MetabolismClinical BiochemistryRetinoic acidTretinoinBiochemistryBasement MembraneCollagen Type ITransforming Growth Factor beta1chemistry.chemical_compoundInternal medicineMalondialdehydemedicineAnimalsRetinoidRNA MessengerRats WistarMolecular BiologyLungPeroxidaseBasement membraneNutrition and DieteticsLungbiologyTumor Necrosis Factor-alphaVitamin A DeficiencyInterleukinsRetinolmedicine.diseaseImmunohistochemistryRatsVitamin A deficiencyPulmonary AlveoliOxidative StressProtein SubunitsEndocrinologymedicine.anatomical_structurechemistryGene Expression RegulationMyeloperoxidasebiology.proteinThe Journal of nutritional biochemistry
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Ambiguous Role of Interleukin-12 in Yersinia enterocolitica Infection in Susceptible and Resistant Mouse Strains

1998

ABSTRACT Endogenous interleukin-12 (IL-12) mediates protection against Yersinia enterocolitica in C57BL/6 mice by triggering gamma interferon (IFN-γ) production in NK and CD4 + T cells. Administration of exogenous IL-12 confers protection against yersiniae in Yersinia -susceptible BALB/c mice but exacerbates yersiniosis in resistant C57BL/6 mice. Therefore, we wanted to dissect the different mechanisms exerted by IL-12 during Yersinia infections by using different models of Yersinia -resistant and -susceptible mice, including resistant C57BL/6 mice, susceptible BALB/c mice, intermediate-susceptible wild-type 129/Sv mice, 129/Sv IFN-γ-receptor-deficient (IFN-γR −/− ) mice and C57BL/6 tumor n…

Yersinia Infectionsmedicine.medical_treatmentImmunologyCD8-Positive T-LymphocytesYersiniaMicrobiologyMicrobiologyProinflammatory cytokineInterferon-gammaMiceTransforming Growth Factor betamedicineAnimalsInterferon gammaYersinia enterocoliticaReceptors InterferonYersinia enterocoliticaMice KnockoutHost Response and InflammationMice Inbred BALB CbiologyTumor Necrosis Factor-alphaYersiniosisbiology.organism_classificationmedicine.diseaseInterleukin-12Killer Cells NaturalMice Inbred C57BLInfectious DiseasesCytokineImmunologyInterleukin 12FemaleParasitologyTumor necrosis factor alphamedicine.drugInfection and Immunity
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An impaired alveolar-capillary barrier in vitro : effect of proinflammatory cytokines and consequences on nanocarrier interaction.

2009

The alveolar region of the lung is an important target for drug and gene delivery approaches. Treatment with drugs is often necessary under pathophysiological conditions, in which there is acute inflammation of the target organ. Therefore, in vitro models of the alveolar-capillary barrier, which mimic inflammatory conditions in the alveolar region, would be useful to analyse and predict effects of novel drugs on healthy or inflamed tissues. The epithelial cell line H441 was cultivated with primary isolated human pulmonary microvascular endothelial cells (HPMECs) or the endothelial cell line ISO-HAS-1 on opposite sides of a permeable filter support under physiological and inflammatory condi…

bilayerPathologytight junctions[SDV.BIO]Life Sciences [q-bio]/Biotechnologymedicine.medical_treatment[SDV]Life Sciences [q-bio]02 engineering and technology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]nanocarrier interactionBiochemistry[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]Electric ImpedancePolyethyleneimineBarrier function0303 health sciencesTight junctionArticlesTransfection021001 nanoscience & nanotechnologyImmunohistochemistryCell biologyEndothelial stem cellCytokine[SDV.TOX]Life Sciences [q-bio]/Toxicology0210 nano-technologyBiotechnologymedicine.medical_specialtyBiomedical EngineeringBiophysicsBioengineering[SDV.BC]Life Sciences [q-bio]/Cellular BiologyGene deliveryBiologyLung injuryModels BiologicalCell LineProinflammatory cytokineBiomaterialsInterferon-gamma03 medical and health sciencesmedicineHumanslung injury030304 developmental biologyAnalysis of VarianceTumor Necrosis Factor-alphaEndothelial CellsBiological TransportCoculture Techniquesalveolar-capillary barrierAlveolar Epithelial CellsNanoparticles
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Functional relevance of soluble TNF-alpha, transmembrane TNF-alpha and TNF-signal transduction in gastrointestinal diseases with special reference to…

2002

As a result of extensive clinical and basic research, the pivotal role of tumour necrosis factor (TNF) in the pathogenesis of chronic inflammatory diseases such as inflammatory bowel disease (IBD) has now generally been acknowledged. This has led to promising clinically effective anti-TNF-strategies. Of note, there is more and more evidence that TNF seems to play a key role in other gastrointestinal diseases including Helicobacter pylori infection, pancreatitis, viral hepatitis and toxic liver damage, too. The action of TNF at the cellular level is mediated by two cell surface receptors, TNF-R1 (p60) and TNF-R2 (p80). The function of these receptors and the downstream intracellular signal t…

business.industryGastrointestinal DiseasesTumor Necrosis Factor-alphamedicine.medical_treatmentGastroenterologyAntibodies MonoclonalProteinsDiseasemedicine.diseaseInflammatory Bowel DiseasesTNF Receptor-Associated Factor 2Inflammatory bowel diseaseTNF Receptor-Associated Factor 1PathogenesisTransduction (genetics)CytokineImmunologyMedicineHumansTumor necrosis factor alphaSignal transductionbusinessReceptorSignal TransductionZeitschrift fur Gastroenterologie
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