Search results for "tumor necrosis factor alpha"

showing 9 items of 479 documents

Oxymetazoline modulates proinflammatory cytokines and the T‐cell stimulatory capacity of dendritic cells

2007

The nasal decongestant oxymetazoline (OMZ) is frequently used in the topical treatment of rhinitis/sinusitis. As proinflammatory cytokines play a critical role in the development and maintenance of local inflammation, the aim of this study was to investigate the influence of OMZ on immune cells in order to diminish the mucosal infiltration of the nose. Peripheral blood mononuclear cells (PBMC) from buffy coats of healthy volunteers were isolated and stimulated in the presence or absence of OMZ. In addition, monocyte-derived dendritic cells (DC) were generated and different concentrations of OMZ were added. DC phenotype and their T-cell stimulatory properties were analysed. The vasoactive su…

oxymetazolinemedicine.medical_treatmentT cellT-LymphocytesInflammationEnzyme-Linked Immunosorbent AssayDermatologyimmunomodulationLymphocyte ActivationBiochemistryProinflammatory cytokinerhinitismedicineHumansAntigen-presenting cellMolecular BiologyCells CulturedDose-Response Relationship Drugbusiness.industryImmunomagnetic SeparationDendritic cellDendritic CellsFlow CytometryNasal decongestantNasal DecongestantsCytokinemedicine.anatomical_structureImmunologyproinflammatory cytokinesLeukocytes MononuclearCytokinesTumor necrosis factor alphaOriginal Articlemedicine.symptombusinessExperimental Dermatology
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Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS.

2005

Phosphorylated p38 mitogen-activated protein kinase (p38MAPK), but not activated c-jun-N-terminal kinase (JNK), increases in the motor neurons of transgenic mice overexpressing ALS-linked SOD1 mutants at different stages of the disease. This effect is associated with a selective increase of phosphorylated MKK3-6, MKK4 and ASK1 and a concomitant upregulation of the TNFalpha receptors (TNFR1 and TNFR2), but not IL1beta and Fas receptors. Activation of both p38 MAPK and JNK occurs in the activated microglial cells of SOD1 mutant mice at the advanced stage of the disease; however, this effect is not accompanied by the concomitant activation of the upstream kinases ASK1 and MKK3,4,6, while both …

p38 mitogen-activated protein kinasesMAP Kinase Kinase 3Mice TransgenicMAP Kinase Kinase 6BiologyMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein KinasesReceptors Tumor Necrosis FactorCellular and Molecular NeuroscienceMiceSuperoxide Dismutase-1Downregulation and upregulationAnimalsHumansASK1RNA Messengerfas ReceptorPhosphorylationReceptorProtein kinase AMolecular BiologyP38MAPK cascadeMotor NeuronsKinaseSuperoxide DismutaseTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisJNK Mitogen-Activated Protein KinasesReceptors Interleukin-1Cell BiologyCell biologyEnzyme ActivationMice Inbred C57BLDisease Models AnimalTumor Necrosis Factor Decoy ReceptorsSpinal CordReceptors Tumor Necrosis Factor Type IDisease ProgressionTumor necrosis factor alphaSignal TransductionMolecular and cellular neurosciences
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TRAIL acts synergistically with iron oxide nanocluster-mediated magneto- and photothermia

2019

International audience; Targeting TRAIL (Tumor necrosis factor (TNF)-Related Apoptosis-Inducing Ligand) receptors for cancer therapy remains challenging due to tumor cell resistance and poor preparations of TRAIL or its derivatives. Herein, to optimize its therapeutic use, TRAIL was grafted onto iron oxide nanoclusters (NCs) with the aim of increasing its pro-apoptotic potential through nanoparticle-mediated magnetic hyperthermia (MHT) or photothermia (PT). Methods: The nanovector, NC@TRAIL, was characterized in terms of size, grafting efficiency, and potential for MHT and PT. The therapeutic function was assessed on a TRAIL-resistant breast cancer cell line, MDA-MB-231, wild type (WT) or T…

photothermal therapyCell SurvivalMedicine (miscellaneous)TRAIL02 engineering and technologyFerric CompoundsFlow cytometryTNF-Related Apoptosis-Inducing LigandCell membrane03 medical and health sciences0302 clinical medicineMicroscopy Electron TransmissionCell surface receptorCell Line Tumormedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologymagnetic hyperthermiaReceptorPharmacology Toxicology and Pharmaceutics (miscellaneous)ComputingMilieux_MISCELLANEOUSchemistry.chemical_classificationCell Deathmedicine.diagnostic_testTumor Necrosis Factor-alphairon oxide nanoclustersapoptosisHyperthermia InducedFlow Cytometry021001 nanoscience & nanotechnology3. Good healthMagnetic hyperthermiamedicine.anatomical_structurechemistryTransferrinApoptosis030220 oncology & carcinogenesisCancer research[SDV.IB]Life Sciences [q-bio]/BioengineeringTumor necrosis factor alpha0210 nano-technologyResearch Paper
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Adrb3 adrenergic receptor is a key regulator of human myometrial apoptosis and inflammation during chorioamnionitis1

2008

The pathophysiology underlying preterm labor triggered by inflammatory conditions such as chorioamnionitis remains largely unclear. It has already been suggested that beta-3 adrenergic (ADRB3) agonists might be of interest in the pharmacological management of preterm labor. Although there is evidence implicating ADRB receptors in the control of inflammation, there are minimal data relating specifically to ADRB3. To explore the cellular consequences of chorioamnionitis and detect apoptosis, we first performed immunostaining and Western blot experiments on human myometrial samples obtained from women with confirmed chorioamnionitis. We then developed an in vitro model of chorioamnionitis by i…

preterm labormedicine.medical_specialtymedicine.medical_treatmentunited-statesbeta-adrenoceptorsStimulationInflammationin-vitroChorioamnionitisProinflammatory cytokineimmunology03 medical and health sciences0302 clinical medicineInternal medicinemedicineInterleukin 8Interleukin 6030304 developmental biology0303 health sciencesbiologycell apoptosislipopolysaccharideapoptosisbacterial infectionCell BiologyGeneral Medicinemedicine.diseasegene-expressioncytokines3. Good healthEndocrinologyCytokineReproductive Medicineinflammation030220 oncology & carcinogenesisbiology.proteincytokine productionbeta(3)-adrenoceptorTumor necrosis factor alphapregnancymedicine.symptomdeliverytumor-necrosis-factorterm
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Inflammatory cytokines shape a changing DNA methylome in monocytes mirroring disease activity in rheumatoid arthritis

2019

Objective: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that mainly targets joints. Monocytes and macrophages are critical in RA pathogenesis and contribute to inflammatory lesions. These extremely plastic cells respond to extracellular signals which cause epigenomic changes that define their pathogenic phenotype. Here, we interrogated how DNA methylation alterations in RA monocytes are determined by extracellular signals. Methods: High-throughput DNA methylation analyses of patients with RA and controls and in vitro cytokine stimulation were used to investigate the underlying mechanisms behind DNA methylation alterations in RA as well as their relationship with clinic…

rheumatoid arthritis0301 basic medicine*DAS28Immunology*disease activityGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineArthritis RheumatoidPathogenesisEpigenome03 medical and health sciences0302 clinical medicineRheumatologymedicineDAS28HumansImmunology and AllergyEpigenomics030203 arthritis & rheumatologyDNA methylationTumor Necrosis Factor-alphabusiness.industryMacrophagesMonocyteTNFaMethylationDNA Methylationmedicine.disease*rheumatoid arthritis030104 developmental biologymedicine.anatomical_structure*TNFaRheumatoid arthritis*DNA methylationImmunologyDNA methylationLeukocytes MononuclearCytokinesTumor necrosis factor alphaInflammation Mediatorsbusinessdisease activityBiomarkersAnnals of the Rheumatic Diseases
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FRI0030 Anti-TNF-α Antibody Targeted To Inflamed Synovial Tissue for The Treatment of Rheumatoid Arthritis

2016

Background TNF-α neutralizing molecules represent one of the most efficient therapeutic approaches to control inflammation in rheumatoid arthritis (RA). The widespread distribution in the body induces the inhibition of TNF-α in all the tissues, requesting the use of high dose of this expensive drug. Another problem that has not yet been solved in the management of RA patients is how to reduce and possibly avoid the side effects, particularly the increased risk of common and opportunistic infections, which may be associated with long-term administration of these therapeutic drugs. Objectives The aim of the present investigation was to show that a recombinant protein obtained by fusing a syno…

rheumatoid arthritisPathologymedicine.medical_specialtyImmunologyArthritisInflammationImmunofluorescenceGeneral Biochemistry Genetics and Molecular BiologyRheumatologyIn vivoAdalimumabmedicineImmunology and AllergyNeutralizing antibodyantigen induced arthritismedicine.diagnostic_testbiologybusiness.industrytarget therapyantigen induced arthritirheumatoid arthritimedicine.diseaseRheumatoid arthritisImmunologyrheumatoid arthritis; antigen induced arthritis; target therapy; immunotherapybiology.proteinTumor necrosis factor alphaimmunotherapymedicine.symptombusinessmedicine.drug
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Rho GTPases Are Involved in the Regulation of NF-κB by Genotoxic Stress

2001

A common cellular response to genotoxic agents and inflammatory cytokines is the activation of NF-kappaB. Here, we addressed the question of whether small GTPases of the Rho family are involved in the stimulation of NF-kappaB signaling by genotoxic agents or TNFalpha in HeLa cells. Inhibition of isoprenylation of Rho proteins by use of the HMG-CoA reductase inhibitor lovastatin attenuated UV-, doxorubicin-, and TNFalpha-induced degradation of IkappaBalpha as well as drug-stimulated DNA binding activity of NF-kappaB. Furthermore, NF-kappaB-regulated gene expression stimulated by either UV irradiation or treatment with TNFalpha was abrogated by lovastatin pretreatment. This indicates that iso…

rho GTP-Binding ProteinsBacterial ToxinsClostridium difficile toxin BGenotoxic StressGTPaseBiologyProinflammatory cytokinechemistry.chemical_compoundBacterial ProteinsNF-KappaB Inhibitor alphamedicineHumansLovastatinTumor Necrosis Factor-alphaNF-kappa BNF-kappa B p50 SubunitNF-κBCell BiologyCell biologyDNA-Binding ProteinsIκBαchemistryDoxorubicinI-kappa B ProteinsTumor necrosis factor alphaLovastatinHeLa CellsSignal Transductionmedicine.drugExperimental Cell Research
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Lovastatin inhibits Rho-regulated expression of E-selectin by TNFalpha and attenuates tumor cell adhesion.

2003

E-selectin mediated cell-cell adhesion plays an important role in inflammatory processes and extravasation of tumor cells. Tumor necrosis factor-alpha (TNF-alpha) induces E-selectin gene and protein expression in primary human endothelial cells (HUVEC) and in an endothelial cell line (EA.hy-926). As shown by ELISA and FACS analyses, HMG-CoA reductase inhibitors (e.g., lovastatin) impair the TNF-alpha stimulated increase in E-selectin protein expression. Similar results were obtained for E-selectin mRNA expression and promoter activity, indicating that the effect of lovastatin is based on inhibition of gene expression. The effective inhibitory concentration of lovastatin was in a physiologic…

rho GTP-Binding ProteinsRHOATranscription GeneticRHOBAntineoplastic AgentsBiochemistryCell MovementCell Line TumorNeoplasmsGene expressionE-selectinGeneticsmedicineCell AdhesionHumansLovastatinCell adhesionMolecular BiologyCells CulturedbiologyTumor Necrosis Factor-alphaCell biologybiology.proteinCancer researchTumor necrosis factor alphaLovastatinEndothelium VascularSignal transductionE-SelectinBiotechnologymedicine.drugSignal TransductionFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Ultraviolet A1 radiation induces nitric oxide synthase-2 expression in human skin endothelial cells in the absence of proinflammatory cytokines.

2001

Skin exposure to ultraviolet radiation from sunlight causes erythema and edema formation as well as inflammatory responses. As some of these ultraviolet-induced effects are potentially mediated by nitric oxide synthases, we examined the role of cytokines and ultraviolet A 1 radiation (340–400 nm) on the expression of the nitric oxide synthase-2 in endothelia of normal human skin biopsies during short-term organ culture as well as expression and activity of the nitric oxide synthase-2 in in vitro cell cultures of human dermal endothelial cells. Both, cytokine challenge (interleukin-1β + tumor necrosis factor-α + interferon-γ) but also ultraviolet A 1 exposure (50 J per cm 2 ) in the absence …

ultraviolet A1Ultraviolet Raysmedicine.medical_treatmentNitric Oxide Synthase Type IIHuman skinInflammationDermatologyBiologyBiochemistryProinflammatory cytokineNitric oxideCell Linechemistry.chemical_compoundInterferon-gammanitric oxidemedicineHumansEndotheliumPromoter Regions GeneticMolecular BiologySkinTumor Necrosis Factor-alphaNitric oxide synthase 2Cell BiologyMolecular biologynitric oxide synthase-2endothelial cellsNitric oxide synthasehealing cytokinesCytokinechemistryEnzyme InductionImmunologybiology.proteinCytokinesTumor necrosis factor alphamedicine.symptomhuman skinInflammation MediatorsNitric Oxide SynthaseInterleukin-1The Journal of investigative dermatology
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