Search results for "Tumor necrosis factor-alpha"

showing 10 items of 504 documents

Haem oxygenase-1 induction reverses the actions of interleukin-1β on hypoxia-inducible transcription factors and human chondrocyte metabolism in hypo…

2013

HO-1 (haem oxygenase-1) catalyses the degradation of haem and possesses anti-inflammatory and cytoprotective properties. The role of inflammatory mediators in the pathogenesis of OA (osteoarthritis) is becoming increasingly appreciated. In the present study, we investigated the effects of HO-1 induction in OA and healthy HACs (human articular chondrocytes) in response to inflammatory cytokine IL-1 β (interleukin-1β) under hypoxic conditions. Hypoxia was investigated as it is a more physiological condition of the avascular cartilage. Hypoxic signalling is mediated by HIFs (hypoxia-inducible factors), of which there are two main isoforms, HIF-1α and HIF-2α. Normal and OA chondrocytes were sti…

Cartilage ArticularMaleSmall interfering RNAmedicine.medical_treatmentInterleukin-1betaBiologyMatrix metalloproteinaseChondrocytesOsteoarthritisBasic Helix-Loop-Helix Transcription FactorsmedicineHumansHypoxiaCollagen Type IITranscription factorAgedTumor Necrosis Factor-alphaCatabolismSOX9 Transcription FactorGeneral MedicineMiddle AgedHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCOPPMatrix MetalloproteinasesCell biologyCytokineBiochemistryFemaleTumor necrosis factor alphamedicine.symptomHeme Oxygenase-1Clinical Science
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Different effects of biological drugs in rheumatoid arthritis

2013

Biological drugs have brought new hope to patients with rheumatoid arthritis (RA) in whom previously existing treatments could not control inflammation, joint destruction, or the progression of disability. The five currently available TNF blockers are approved for treating RA patients, but they have different structures, morphology, pharmacokinetic properties, and activity. Randomised clinical trials (RCTs) have shown that they improve the signs and symptoms of both early and long-standing RA and other inflammatory arthritides, prevent radiographic progression, and improve the patients' health-related quality of life. However, they are more effective in combination with methotrexate (MTX) t…

Cartilage Articularmedicine.medical_specialtyDrug-Related Side Effects and Adverse ReactionsImmunologyArthritisPharmacologyArthritis Rheumatoidchemistry.chemical_compoundChondrocytesPharmacotherapyTocilizumabDrug TherapyRheumatoidInternal medicinemedicineHumansImmunology and AllergyArthritis Rheumatoid; Cartilage Articular; Chondrocytes; Drug Therapy Combination; Drug-Related Side Effects and Adverse Reactions; Humans; Inflammation Mediators; Pharmaceutical Preparations; Randomized Controlled Trials as Topic; Tumor Necrosis Factor-alphaAdverse effectRandomized Controlled Trials as TopicTumor Necrosis Factor-alphabusiness.industryArthritisAbataceptmedicine.diseaseClinical trialCartilagePharmaceutical PreparationschemistryRheumatoid arthritisCombinationDrug Therapy CombinationRituximabInflammation MediatorsbusinessArticularmedicine.drugAutoimmunity Reviews
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A novel SP-1 site in the human interleukin-1β promoter confers preferential transcriptional activity in keratinocytes

1996

To investigate the mechanisms of transcriptional activation of interleukin-1beta (IL-1beta) in non-monocytic cells, we constructed a series of reporter plasmids with the bacterial chloramphenicol acetyltransferase gene linked to various parts of the human IL-1beta promoter and performed transient transfection experiments. We identified a promoter segment that activates transcription most efficiently in keratinocytes. Electrophoretic mobility shift assays (EMSA) with a 43-mer oligonucleotide derived from the functionally identified cis-acting element revealed specific complexes. By competition analysis with transcription factor consensus sequence oligonucleotides and by immunosupershift, tra…

Cell NucleusKeratinocytesTranscriptional ActivationSp1 transcription factorTranscription GeneticSp1 Transcription FactorTumor Necrosis Factor-alphaImmunologyResponse elementBiologyMolecular biologyMonocytesChloramphenicol acetyltransferaseGenes ReporterTranscription (biology)MutationConsensus sequenceTranscriptional regulationHumansImmunology and AllergyPromoter Regions GeneticTranscription factorGeneCell Line TransformedInterleukin-1European Journal of Immunology
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PECAM-1 expression in human mesothelial cells: an in vitro study.

1996

Mesothelial cells are actively involved in inflammatory processes by expressing a set of cell adhesion molecules (CAMs). Transmigration of leukocytes into inflamed tissues requires a chemotactic stimulus and engagement of platelet-endothelial cell adhesion molecule-1 (PECAM-1). To investigate the kinetics involved in peritonitis, pure cultures of mesothelial cells are necessary. In previous studies, we have found that human mesothelial cells (HOMES) show a weak constitutive expression of PECAM-1, which cannot be further stimulated by cytokines. It is known that all serous cavities and body fluids contain numerous macrophages which strongly express this adhesion molecule. To identify the cel…

Cell SeparationIn Vitro TechniquesEpitheliumPathology and Forensic MedicineInterferon-gammaE-selectinmedicineHumansCell adhesionMolecular BiologyCells CulturedbiologyChemistryCell adhesion moleculeTumor Necrosis Factor-alphaMonocyteEpithelial CellsCell BiologyGeneral MedicineCell sortingMolecular biologyImmunohistochemistryRecombinant ProteinsCell biologyPlatelet Endothelial Cell Adhesion Molecule-1Microscopy Electronmedicine.anatomical_structureCell culturebiology.proteinNeural cell adhesion moleculeOmentumMesothelial CellInterleukin-1Pathobiology : journal of immunopathology, molecular and cellular biology
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mRNA-induction and cytokine release during in vitro exposure of human nasal respiratory epithelia to methyl methacrylate

2007

Abstract Background Methyl methacrylate (MMA) has been reported to cause histopathological changes in rodent nasal epithelium after inhalation challenges. Data in humans are lacking. Methods In this in vitro design 22 primary cell cultures taken from inferior turbinate tissue of healthy individuals were exposed to MMA concentrations of 50 ppm (German MAK-value) and 200 ppm. mRNA expression and cytokine release of inflammatory mediators were quantified after 4 h and after 24 h. Controls were exposed to synthetic air. Q-PCR analysis was performed for TNF-α, IL-1β, IL-6, IL-8, MCP-1, GMCSF, Cox-1 and Cox-2. ELISA assays were performed from culture supernatants for TNF-α, IL-1β, IL-6, IL-8, MCP…

Cell Survivalmedicine.medical_treatmentCell Culture TechniquesEnzyme-Linked Immunosorbent AssayInflammationMethylmethacrylateBiologyToxicologyAndrologyDownregulation and upregulationmedicineHumansRNA MessengerRespiratory systemCells CulturedChemokine CCL2Dose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaInterleukinsGranulocyte-Macrophage Colony-Stimulating FactorAntimutagenic AgentsEpithelial CellsGeneral MedicineEpitheliumIn vitroNasal MucosaDose–response relationshipCytokinemedicine.anatomical_structureGene Expression RegulationCyclooxygenase 2Cell cultureImmunologyCyclooxygenase 1Cytokinesmedicine.symptomToxicology Letters
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Intrinsic TNFR2 signaling in T regulatory cells provides protection in CNS autoimmunity

2018

Significance In spite of TNF involvement in the pathogenesis of multiple sclerosis (MS), systemic TNF neutralization in MS patients was not successful. One of the possible reasons is that TNF possesses both pathogenic and protective features that may be related to TNFR1 versus TNFR2 receptor engagement. This study uncovers one of such protective functions of TNF mediated by intrinsic TNFR2 signaling in Treg cells. In mice bearing humanized TNF and TNFR2 genetic loci, TNFR2 ablation restricted to Treg cells led to reduced capacity to control Th17 cell responses, exacerbated experimental autoimmune encephalomyelitis (EAE) development, and affected the maintenance of Treg cells. These findings…

Central Nervous System0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT regulatory cellsmedicine.medical_treatmentAutoimmunitychemical and pharmacologic phenomenaBiologymedicine.disease_causeT-Lymphocytes RegulatoryneuroinflammationAutoimmunityMice03 medical and health sciencesImmunology and Inflammation0302 clinical medicineImmune systemmedicineAnimalsHumansReceptors Tumor Necrosis Factor Type IIIL-2 receptorCells CulturedNeuroinflammationMice KnockoutAutoimmune diseaseMultidisciplinaryEAETumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisFOXP3hemic and immune systemsBiological Sciencesmedicine.diseaseTNF/TNFR2Mice Inbred C57BLDisease Models Animalhumanized mice030104 developmental biologyCytokineGene Expression RegulationImmunology030215 immunologyProceedings of the National Academy of Sciences
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Genetic Cell Ablation Reveals Clusters of Local Self-Renewing Microglia in the Mammalian Central Nervous System

2015

SummaryDuring early embryogenesis, microglia arise from yolk sac progenitors that populate the developing central nervous system (CNS), but how the tissue-resident macrophages are maintained throughout the organism’s lifespan still remains unclear. Here, we describe a system that allows specific, conditional ablation of microglia in adult mice. We found that the microglial compartment was reconstituted within 1 week of depletion. Microglia repopulation relied on CNS-resident cells, independent from bone-marrow-derived precursors. During repopulation, microglia formed clusters of highly proliferative cells that migrated apart once steady state was achieved. Proliferating microglia expressed …

Central Nervous SystemCellular differentiationCentral nervous systemInterleukin-1betaImmunologyCX3C Chemokine Receptor 1Bone Marrow CellsBiologyMiceCell MovementCX3CR1medicineAnimalsImmunology and AllergyProgenitor cellNeuroinflammationCell ProliferationReceptors Interleukin-1 Type IMicrogliaBase SequenceTumor Necrosis Factor-alphaMacrophagesCell DifferentiationSequence Analysis DNAHematopoietic Stem CellsCell biologyMice Inbred C57BLmedicine.anatomical_structureInfectious DiseasesImmunologyTumor necrosis factor alphaReceptors ChemokineMicrogliaSignal transductionSignal TransductionImmunity
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Interaction of inflammation, thrombosis, aspirin and enoxaparin in CNS experimental antiphospholipid syndrome

2008

Experimental antiphospholipid syndrome (eAPS) induced by immunization with beta(2)-glycoprotein I (beta(2)-GPI) causes behavioral hyperactivity. We assessed the role of thrombotic and inflammatory perivascular factors and standard APS therapies for CNS manifestations. Groups of mice (n=10 per group) were immunized once with beta(2)-GPI (eAPS) or adjuvant (controls) and treated daily from 1 month after immunization with either sham injections, aspirin (1.2 mg/kg) or enoxaparin (1 mg/kg) for 3 months. Serum antiphospholipid antibodies (aPL) and brain levels of tissue necrosis factor-alpha (TNF-alpha) and prostaglandin E (PGE) were then measured by ELISA and thrombin inhibitors by immunoblot. …

Central Nervous Systemmedicine.medical_treatmentEnzyme-Linked Immunosorbent AssayInflammationPharmacologylcsh:RC321-571AnticoagulationMiceFibrinolytic AgentsAntiphospholipid syndromeAnimalsMedicineBeta 2-Glycoprotein IAlprostadilEnoxaparinlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryPhospholipidsInflammationBehaviorAnalysis of VarianceMice Inbred BALB CAspirinAspirinBehavior AnimalTumor Necrosis Factor-alphabusiness.industryThrombosisAntiphospholipid Syndromemedicine.diseaseThrombosisAnimal modelsDisease Models AnimalNeurologybeta 2-Glycoprotein IImmunologyExploratory BehaviorFemaleTumor necrosis factor alphamedicine.symptombusinessDiscovery and development of direct thrombin inhibitorsProstaglandin Emedicine.drugNeurobiology of Disease
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Activation of PPARβ/δ inhibits leukocyte recruitment, cell adhesion molecule expression, and chemokine release

2009

Abstract Activation of the nuclear receptor PPARb/d inhibits acute inflammatory responses in vitro with human primary cells and in vivo by targeting the endothelial cell-leukocyte interaction. The infiltration of PMNs into tissues is a prominent feature in inflammation. The mechanism underlying PMN recruitment depends on the release of chemotactic mediators and CAM expression on endothelial cells. The nuclear receptor PPARβ/δ is widely expressed in many tissues, including the vascular endothelium; however, its role in acute inflammation remains unclear. Using intravital microscopy in the mouse cremasteric microcirculation, we have shown that activation of PPARβ/δ by its selective ligand GW5…

ChemokineEndotheliumImmunologyGene ExpressionLeukocyte RollingInflammationMicrocirculationMicemedicineAnimalsImmunology and AllergyLeukocyte RollingPPAR deltaMuscle SkeletalPPAR-betaInflammationMicroscopy VideobiologyTumor Necrosis Factor-alphaCell adhesion moleculeMicrocirculationCell BiologyCell biologyChemotaxis Leukocytemedicine.anatomical_structurebiology.proteinPeroxisome proliferator-activated receptor deltaChemokinesmedicine.symptomCell Adhesion MoleculesIntravital microscopyJournal of Leukocyte Biology
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The fungal lactone oxacyclododecindione is a potential new therapeutic substance in the treatment of lupus-associated kidney disease.

2013

Recently oxacyclododecindione (Oxa), a macrocyclic lactone isolated from the imperfect fungus Exserohilum rostratum, has been described as a potent transcription inhibitor of inducible proinflammatory and profibrotic genes in cell culture models. As kidney disease in systemic lupus erythematosus is characterized by aberrant expression of inflammatory mediators and infiltration of immune cells, we investigated the effect of Oxa in MRL-Fas(lpr) mice, a model of systemic lupus erythematosus. These mice develop a spontaneous T-cell and macrophage-dependent autoimmune disease including severe glomerulonephritis that shares features with human lupus. Comparable to the results of in vitro models, …

ChemokineMice Inbred MRL lprMacrocyclic CompoundsAnti-Inflammatory AgentsProtein Array AnalysisGene ExpressionInflammationChemokine CXCL9Proinflammatory cytokineInterferon-gammaMiceImmune systemmedicineAnimalsCalgranulin ARNA MessengerChemokine CCL4Chemokine CCL5Chemokine CCL2Autoimmune diseaseSystemic lupus erythematosusbiologyInterleukin-6Tumor Necrosis Factor-alphaGlomerulonephritismedicine.diseaseLupus NephritisChemokine CXCL12Disease Models AnimalNephrologyImmunologybiology.proteinCytokinesFemaleOsteopontinmedicine.symptomKidney diseaseKidney international
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