Search results for "tumor necrosis factor alpha"

showing 10 items of 479 documents

Altered expression of inflammation-related genes in human carotid atherosclerotic plaques.

2011

Abstract Objective Inflammation is a pivotal process in atherosclerosis development and progression, but the underlying molecular mechanisms remain largely obscure. We have conducted an extensive expression study of atherosclerotic plaques to identify the inflammatory pathways involved in atherosclerosis. Methods We studied 11 human carotid plaques, their respective adjacent regions and 7 control arteries from different subjects. Expression of 92 genes was studied by TaqMan low-density array human inflammation panel. Human aortic endothelial and smooth muscle cells were used for in vitro experiments. Results The mRNA levels of 44/92 genes (48%) differed significantly between the tissues exa…

Carotid Artery DiseasesMalemedicine.medical_specialtyMyocytes Smooth MuscleReceptors ProstaglandinPTGS1InflammationReceptors EpoprostenolSettore MED/22 - Chirurgia VascolareMuscle Smooth VascularCytochrome P-450 Enzyme SystemInternal medicineGene expressionmedicineHumansRNA MessengerReceptors CytokineCells CulturedAgedRegulation of gene expressionInflammationbiologyTumor Necrosis Factor-alphaGene Expression ProfilingMacrophagesEndothelial CellsMiddle AgedCoculture TechniquesPlaque AtheroscleroticGene expression profilingLipoproteins LDLEndocrinologyEicosanoidEicosanoid pathwayGene Expression RegulationItalyAtherosclerosiCase-Control StudiesArachidonate 5-lipoxygenasebiology.proteinCancer researchOxidative streTumor necrosis factor alphaFemaleGene expressionmedicine.symptomInflammation MediatorsCardiology and Cardiovascular MedicineCell Adhesion MoleculesAtherosclerosis
researchProduct

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
researchProduct

Cladribine exerts an immunomodulatory effect on human and murine dendritic cells

2014

Cladribine is a purine nucleoside analog developed to treat lymphoid malignancies. Reported therapeutic benefits for the autoimmune disease multiple sclerosis indicate additional immunomodulatory effects beyond the well-characterized cytotoxic activity causing lymphopenia. Here, we demonstrate that cladribine reduces the secretion of inflammatory cytokines and chemokines by murine and human dendritic cells, the most potent antigen-presenting cells. This compound also modulates the expression of the activation markers CD86 and MHC II. Furthermore, cladribine affects the T cell priming capacity of dendritic cells, resulting in reduced induction of interferon-γ- and tumor necrosis factor-α-pro…

Cell SurvivalT-LymphocytesT cellImmunologyBiologyMicePhagocytosismedicineAnimalsHumansImmunologic FactorsImmunology and AllergyCytotoxic T cellAntigen-presenting cellCladribineCells CulturedCell ProliferationPharmacologyCD86ChemotaxisCell DifferentiationDextransDendritic CellsDendritic cellmedicine.diseaseMice Inbred C57BLLeukemiamedicine.anatomical_structureImmunologyLeukocytes MononuclearCancer researchCladribineCytokinesTumor necrosis factor alphaFluorescein-5-isothiocyanatemedicine.drugInternational Immunopharmacology
researchProduct

Characteristic ERK1/2 signaling dynamics distinguishes necroptosis from apoptosis

2021

International audience; ERK1/2 involvement in cell death remains unclear, although many studies have demonstrated the importance of ERK1/2 dynamics in determining cellular re- sponses. To untangle how ERK1/2 contributes to two cell death programs, we investigated ERK1/2 signaling dynamics during hFasL-induced apoptosis and TNF-induced necroptosis in L929 cells. We observed that ERK1/2 inhibition sensi- tizes cells to apoptosis while delaying necroptosis. By monitoring ERK1/2 activity by live-cell imaging using an improved ERK1/2 biosensor (EKAR4.0), we reported differential ERK1/2 signaling dynamics between cell survival, apoptosis, and nec- roptosis. We also decrypted a temporally shifted …

Cell biologyProgrammed cell deathScience[SDV]Life Sciences [q-bio]Necroptosis[SDV.BBM.BP] Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsPROTEINMECHANISMSESCRTACTIVATION03 medical and health sciences0302 clinical medicineINFLAMMATIONGene expressionMedicine and Health SciencesKINASEBiology030304 developmental biology0303 health sciencesMultidisciplinaryIDENTIFICATIONChemistryNECROSISQDynamics (mechanics)Biology and Life SciencesErk1 2 signalingCell biology[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biophysics[SDV] Life Sciences [q-bio]Biological sciencesBiomolecular engineeringCELL-DEATHApoptosisCell culture030220 oncology & carcinogenesisTumor necrosis factor alphaBIOSENSORSHuman medicineiScience
researchProduct

P043 Succinate receptor (SUCNR1) mediates leukocyte-endothelial cell interactions induced by TNFa

2021

Abstract Background The Krebs cycle metabolite succinate contributes to inflammatory conditions like arthritis and colitis by activating its receptor SUCNR1. We aimed to analyze whether the succinate-SUCNR1 pathway contributes to the leukocyte-endothelial cell interactions that initiate the inflammatory response. Methods We evaluated leukocyte rolling and adhesion by intravital microscopy in cremaster venules of wild-type (WT) and Sucrn1−/− mice treated, 4h before, with succinate (1 Mm, intraescrotally), combined or not with the common pro-inflammatory cytokine TNFα (500 ng/mice, i.p.), or with their vehicles. We analyzed the activity of the NF-κB signaling pathway in endothelial cells (HUV…

Cell signalingEndotheliumbusiness.industrymedicine.medical_treatmentGastroenterologyInflammationGeneral MedicineCell biologyEndothelial stem cellCytokinemedicine.anatomical_structuremedicineTumor necrosis factor alphamedicine.symptomSignal transductionReceptorbusinessJournal of Crohn's and Colitis
researchProduct

Effects of Cytokines on the Expression of Cell Adhesion Molecules by Cultured Human Omental Mesothelial Cells

1995

Cultured mesothelial cells (HOMES) are very responsive to the proinflammatory cytokines, interleukin (IL)-1 and tumor necrosis factor-alpha (TNF-alpha). E-selectin, ICAM-1 and VCAM-1 are known to play an important role, because they are presented by diverse cell types, for example endothelial cells (ECs), and interact with co-responding ligands on white blood cell membranes. In this study, the expression of ICAM-1, VCAM-1, E-selectin as well as PECAM-1 on cultured HOMES was studied over 5, 24, 48 and 72 h exposure to IL-1 beta, interferon-gamma and TNF-alpha. In previous studies we have shown that IL-1 beta and TNF-alpha increase the expression of ICAM-1, E-selectin and VCAM-1 on the cytopl…

Cell typeTime Factorsmedicine.medical_treatmentUmbilical veinImmunophenotypingPathology and Forensic MedicineProinflammatory cytokineImmunoenzyme TechniquesmedicineHumansFluorescent Antibody Technique IndirectMolecular BiologyCells CulturedChemistryCell adhesion moleculeInterleukinEpithelial CellsCell BiologyGeneral MedicineIntercellular Adhesion Molecule-1Cell biologyPlatelet Endothelial Cell Adhesion Molecule-1CytokineMicroscopy FluorescenceCell cultureCytokinesTumor necrosis factor alphaE-SelectinCell Adhesion MoleculesOmentumPathobiology
researchProduct

Dihydrocucurbitacin B Inhibits Delayed Type Hypersensitivity Reactions by Suppressing Lymphocyte Proliferation

2007

We have studied the effects of dihydrocucurbitacin B, a triterpene isolated from Cayaponia tayuya roots, on different models of delayed type hypersensitivity (DTH) in mice, as well as on T-lymphocyte proliferation and the mediators involved. In experiments with mice, dihydrocucurbitacin B inhibited the inflammatory reactions induced by oxazolone, dinitrofluorobenzene, and sheep red blood cells, reducing both the edema and cell infiltration. Moreover, the analysis of inflamed tissues showed that dihydrocucurbitacin B reduced the presence of the most relevant cytokines implicated in these processes, including interleukin-1 beta, interleukin-4, and tumor necrosis factor-alpha. Dihydrocucurbita…

CellLymphocyte proliferationLymphocyte ActivationResting Phase Cell CycleOxazoloneMicechemistry.chemical_compoundCyclinsmedicineAnimalsHypersensitivity DelayedCyclinInflammationPharmacologyNFATC Transcription FactorsbiologyNFATCell cyclebiology.organism_classificationMolecular biologyTriterpenesCayaponia tayuyaDisease Models Animalmedicine.anatomical_structurechemistryImmunologyCytokinesMolecular MedicineTumor necrosis factor alphaJournal of Pharmacology and Experimental Therapeutics
researchProduct

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
researchProduct

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
researchProduct

Neural inflammation alters synaptic plasticity probed by 10 Hz repetitive magnetic stimulation

2020

ABSTRACTSystemic inflammation is associated with alterations in complex brain functions such as learning and memory. However, diagnostic approaches to functionally assess and quantify inflammation-associated alterations in synaptic plasticity are not well-established. In previous work, we demonstrated that bacterial lipopolysaccharide (LPS)-induced systemic inflammation alters the ability of hippocampal neurons to express synaptic plasticity, i.e., the long-term potentiation (LTP) of excitatory neurotransmission. Here, we tested whether synaptic plasticity induced by repetitive magnetic stimulation (rMS), a non-invasive brain stimulation technique used in clinical practice, is affected by L…

ChemistryBrain stimulationSynaptic plasticityExcitatory postsynaptic potentialStimulationTumor necrosis factor alphaLong-term potentiationNeurotransmissionHippocampal formationNeuroscience
researchProduct