Search results for "tumor necrosis factor alpha"

showing 10 items of 479 documents

Epigenetic control of IL-23 expression in keratinocytes is important for chronic skin inflammation

2018

The chronic skin inflammation psoriasis is crucially dependent on the IL-23/IL-17 cytokine axis. Although IL-23 is expressed by psoriatic keratinocytes and immune cells, only the immune cell-derived IL-23 is believed to be disease relevant. Here we use a genetic mouse model to show that keratinocyte-produced IL-23 is sufficient to cause a chronic skin inflammation with an IL-17 profile. Furthermore, we reveal a cell-autonomous nuclear function for the actin polymerizing molecule N-WASP, which controls IL-23 expression in keratinocytes by regulating the degradation of the histone methyltransferases G9a and GLP, and H3K9 dimethylation of the IL-23 promoter. This mechanism mediates the inducti…

KeratinocytesMale0301 basic medicinemedicine.medical_treatmentWiskott-Aldrich Syndrome Protein NeuronalGeneral Physics and AstronomyEpigenesis GeneticHistonesMice0302 clinical medicineGenes ReporterInterleukin 23Promoter Regions Geneticlcsh:ScienceSkinMice KnockoutMultidisciplinaryInterleukin-17QMiddle AgedCytokine030220 oncology & carcinogenesisHistone methyltransferaseTumor necrosis factor alphaSignal transductionmedicine.symptomSignal TransductionAdultScienceGreen Fluorescent ProteinsPrimary Cell CultureInflammationBiologyArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesImmune systemPsoriasismedicineAnimalsHumansPsoriasisInflammationHistone-Lysine N-MethyltransferaseGeneral Chemistrybiochemical phenomena metabolism and nutritionmedicine.diseaseDisease Models AnimalHEK293 Cells030104 developmental biologyInterleukin-23 Subunit p19Cancer researchlcsh:QNature Communications
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Potential antipsoriatic effect of chondroitin sulfate through inhibition of NF-κB and STAT3 in human keratinocytes

2012

Abstract Chondroitin sulfate (CS) is a natural glycosaminoglycan, formed by the 1–3 linkage of d -glucuronic acid to N-acetylgalactosamine, present in the extracellular matrix. It is used as a slow acting disease modifying agent in the treatment of osteoarthritis, and part of its beneficial effects are due to its antiinflammatory properties that result from an inhibitory effect on NF-κB signaling pathway. This ability raises the hypothesis that CS might be effective in other chronic inflammatory processes such as psoriasis, in which a deregulation of NF-κB is a key feature. In addition, psoriasis is characterized by an upregulation of STAT3 signaling pathway that is related to the epidermal…

KeratinocytesSTAT3 Transcription FactorBlotting WesternPrimary Cell CultureAnti-Inflammatory AgentsDermoscopyElectrophoretic Mobility Shift AssayPharmacologyStat3 Signaling Pathwaychemistry.chemical_compoundDownregulation and upregulationPsoriasismedicineHumansPsoriasisChondroitin sulfateCells CulturedPharmacologyChemistryChondroitin SulfatesNF-kappa BNF-κBmedicine.diseaseMicroscopy FluorescenceImmunologyPhosphorylationTumor necrosis factor alphaSignal transductionProtein BindingPharmacological Research
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Studies of Jak/STAT3 expression and signalling in psoriasis identifies STAT3-Ser727 phosphorylation as a modulator of transcriptional activity

2013

Jak/Tyk proteins have recently aroused as possible therapeutic targets for the treatment of psoriasis. In psoriasis, these proteins signal through STAT molecules including STAT3, and STAT3 expression and activation has been shown augmented in psoriatic lesions. Here, we characterized the expression of Jak/Tyk proteins in lesional compared with non-lesional psoriatic skin. Jak1, Jak2 mRNA and protein and Tyk2 mRNA appeared to be downregulated, whereas Jak3 mRNA expression was increased. Moreover, STAT3 expression and activation was examined in psoriasis. STAT3 is activated at two phosphorylation sites: Tyr705 and Ser727. Both phosphorylation sites were phosphorylated in lesional psoriatic sk…

KeratinocytesSTAT3 Transcription FactorTranscription GeneticMAP Kinase Signaling SystemBiopsyp38 mitogen-activated protein kinasesPrimary Cell CultureGene ExpressionDermatologyBiochemistrystatInterleukin 20PsoriasisSerinemedicineHumansPsoriasisRNA MessengerPhosphorylationSTAT3Molecular BiologySkinTYK2 KinasebiologyInterleukin-6InterleukinsJanus Kinase 3Janus Kinase 1Janus Kinase 2medicine.diseaseTyrosine kinase 2biology.proteinCancer researchPhosphorylationTumor necrosis factor alphaSignal Transduction
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Avarol inhibits TNF-a generation and NF-kB activation in human cells and in animal models

2007

Avarol is a marine sesquiterpenoid hydroquinone with interesting pharmacological properties including anti-inflammatory and antipsoriatic effects. In the present study we evaluated the pharmacological effect of avarol on some inflammatory parameters related to the pathogenesis of psoriasis. Avarol inhibited tumor necrosis factor-alpha (TNF-alpha) generation in stimulated human monocytes (IC(50) 1 microM) and TNF-alpha-induced activation of nuclear factor-kappaB (NF-kappaB)-DNA binding in keratinocytes. In the mouse air pouch model, administration of avarol produced a dose-dependent reduction of TNF-alpha generation (ED(50) 9.2 nmol/pouch) as well as of interleukin (IL)-1beta, prostaglandin …

Keratinocytesmedicine.medical_specialtymedicine.medical_treatmentAnti-Inflammatory AgentsAntineoplastic AgentsBiologyPharmacologyMonocytesGeneral Biochemistry Genetics and Molecular BiologyCell LineMicechemistry.chemical_compoundDownregulation and upregulationIn vivoInternal medicinemedicineAnimalsHumansPsoriasisGeneral Pharmacology Toxicology and PharmaceuticsPeroxidaseInflammationHyperplasiaDose-Response Relationship DrugTumor Necrosis Factor-alphaNF-kappa B p50 SubunitInterleukinNF-κBGeneral MedicineDisease Models AnimalEndocrinologymedicine.anatomical_structureEicosanoidchemistryTetradecanoylphorbol AcetateFemaleTumor necrosis factor alphaEpidermisInflammation MediatorsKeratinocyteSesquiterpenesProstaglandin E
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Induction of inflammatory cytokines in murine keratinocytes upon in vivo stimulation with contact sensitizers and tolerizing analogues

1992

In order to elucidate the role of keratinocytes (KCs) in the induction of contact sensitivity, we applied various contact sensitizers [2,4-dinitrofluorobenzene (DNFB), urushiol, 3-n-pentadecylcatechol (PDC), 4-ethoxymethylene-2-phenyloxazol-5-one (oxazolone)] and tolerizing compounds [2,4-dinitrothiocyanobenzene (DNTB), 5-methyl-3-n-pentadecyl-catechol (5-Me-PDC)] onto the earskin of non-sensitized Balb/c mice. In addition, we applied croton oil as a non-sensitizing, but stimulatory agent. Cytokine production was demonstrated by Northern blot hybridization of the total cellular RNA extracted from epidermal cells depleted by Langerhans cells and Thy 1+ dendritic cells using radiolabeled DNA …

Keratinocytesmedicine.medical_treatmentAlpha (ethology)DermatologyBiologyDermatitis ContactBiochemistryProinflammatory cytokineMiceIn vivomedicineAnimalsCroton oilRNA MessengerMicroscopy ImmunoelectronMolecular BiologyCells CulturedMice Inbred BALB CEpidermis (botany)Tumor Necrosis Factor-alphaEarBlotting NorthernImmunohistochemistryMolecular biologyStimulation ChemicalTolerance inductionCytokineImmunologyCytokinesTumor necrosis factor alphaInterleukin-1Experimental Dermatology
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Tumor necrosis factor-receptor 2 is up-regulated on lamina propria T cells in Crohn's disease and promotes experimental colitis in vivo

2002

Tumor necrosis factor (TNF) plays a pivotal role in the pathogenesis of Crohn's disease (CD). However, little is known about the role of TNF receptors (TNF-R) in this disease. Here, we found that TNF-R2 (in contrast to TNF-R1) was significantly up-regulated on lamina propria and peripheral blood T cells in CD compared to control patients. To directly test the functional role of TNF-R2 in Th1-mediated experimental colitis in vivo, we took advantage of transgenic animals overexpressing TNF-R2 in T cells. Reconstitution of SCID mice with CD4+ CD62L+ T cells from TNF-R2 transgenic mice led to an earlier wasting syndrome, a more severe colitis and augmented Th1 cytokine production than reconstit…

Lamina propriamedicine.medical_treatmentImmunologyT lymphocyteBiologyPeripheral blood mononuclear cellInterleukin 21medicine.anatomical_structureCytokineImmunologymedicineCancer researchImmunology and AllergyTumor necrosis factor alphaTumor necrosis factor receptor 2ReceptorEuropean Journal of Immunology
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Leptin: A pivotal mediator of intestinal inflammation in mice

2002

Abstract Background & Aims: In addition to acting as a regulator of food intake and energy expenditure, leptin can also modulate immune and inflammatory responses. The role of leptin in intestinal inflammation is the focus of the present study. Methods: Acute and chronic colitis were induced in leptin-deficient ob/ob or wild-type (WT) mice using dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS). The severity of colitis was evaluated, and possible mechanisms were studied. Results: Leptin directly stimulates intraepithelial lymphocytes (IELs) and lamina propria mononuclear cells (LPMCs). In the DSS acute model, ob/ob mice exhibited a 72% reduction of colitis severity and sp…

LeptinSTAT3 Transcription Factormedicine.medical_specialtyColonanimal diseasesdigestive systemMonocytesProinflammatory cytokineMiceReference ValuesInternal medicinemedicineAnimalsInterferon gammaLymphocytesObesityIntestinal MucosaColitisMacrophage inflammatory proteinCells CulturedLeptin DeficiencyHepatologybusiness.industryLeptinDextran SulfateGastroenterologyColitismedicine.diseasedigestive system diseasesDNA-Binding ProteinsIsoenzymesMice Inbred C57BLEndocrinologyTrinitrobenzenesulfonic AcidCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesEnzyme InductionChronic DiseaseImmunologyTrans-ActivatorsCytokinesIntraepithelial lymphocyteFemaleTumor necrosis factor alphaDisease SusceptibilityChemokinesbusinessmedicine.drugGastroenterology
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Anti-inflammatory effects of annexin-1: stimulation of IL-10 release and inhibition of nitric oxide synthesis.

2003

Annexin-1 (ANX-1) is an anti-inflammatory protein induced by glucocorticoids. Like glucocorticoids, ANX-1 and derived peptides inhibit eicosanoid synthesis, block leukocyte migration and induce apoptosis of inflammatory cells. Cytokines may possess either pro-inflammatory, i.e. interleukin(IL)-1beta, tumor necrosis factor (TNF)-alpha, IL-12 or anti-inflammatory properties, i.e. IL-4, IL-10. The experiments described in the present study have been performed to answer the question whether the anti-inflammatory action of ANX-1 may be mediated, at least in part, by the release of IL-10. In macrophage (J774) cell line cultures primed with lipolysaccharide (LPS), recombinant ANX-1 stimulated IL-1…

Leukocyte migrationCell SurvivalImmunologyAnti-Inflammatory AgentsNitric Oxide Synthase Type IINitric OxideNitric oxideCell Linechemistry.chemical_compoundMiceAnnexinImmunology and AllergyAnimalsRNA MessengerEnzyme InhibitorsAnnexin A1PharmacologybiologyReverse Transcriptase Polymerase Chain ReactionMacrophagesInterleukinPeptide FragmentsRecombinant ProteinsCell biologyInterleukin-10Nitric oxide synthasechemistryBiochemistryApoptosisbiology.proteinTumor necrosis factor alphaNitric Oxide SynthaseAnnexin A1International immunopharmacology
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Beneficial effects of heme oxygenase-1 up-regulation in the development of experimental inflammation induced by zymosan.

2003

Heme oxygenase-1 (HO-1) is part of the integrated response to oxidative stress. This enzyme may exert anti-inflammatory effects in some animal models, although the precise mechanisms are not fully understood. We have examined the role of HO-1 in the inflammatory response induced by zymosan in the mouse air pouch. Zymosan administration induced HO-1 protein expression in leukocytes migrating to exudates, with maximal levels in the late phase of this response (24-48 h). This was accompanied by ferritin induction and bilirubin accumulation, indicating that this enzyme is active in our model. HO-1 expression by zymosan treatment was partly reduced by aminoguanidine, suggesting the participation…

Leukotriene B4Blotting WesternInflammationCell CountPharmacologymedicine.disease_causeLeukotriene B4Dinoprostonechemistry.chemical_compoundMicePhagocytosismedicineAnimalsHemePharmacologyInflammationTumor Necrosis Factor-alphaMacrophagesZymosanZymosanMembrane ProteinsBilirubinExudates and TransudatesFlow CytometryUp-RegulationHeme oxygenasechemistryBiochemistryHeme Oxygenase (Decyclizing)Molecular MedicineCytokinesEicosanoidsHeminTumor necrosis factor alphaFemalemedicine.symptomOxidative stressCell DivisionHeme Oxygenase-1HeminInterleukin-1The Journal of pharmacology and experimental therapeutics
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Voluntary distance running prevents TNF-mediated liver injury in mice through alterations of the intrahepatic immune milieu

2017

AbstractPhysical activity confers a broad spectrum of health benefits. Beyond the obvious role in metabolically driven diseases, the role of physical activity in acute liver injury is poorly explored. To study the role of physical activity in acute liver injury, a novel model of voluntary distance running in mice was developed and mice were subjected to acute liver injury induced by N-galactosamine (GalN) and lipopolysaccharide (LPS). Analyses included histological stains, immunoblotting, qRT-PCR and FACS analysis. Voluntary distance running increased to an average of 10.3 km/day after a learning curve. Running lead to a decrease in the absolute numbers of intrahepatic CD4+ T and B lymphocy…

Lifestyle modification0301 basic medicineLipopolysaccharidesMaleCancer ResearchChemokineApoptosisGalactosamineLiver Function TestsAlarminsLiver injurybiologymedicine.diagnostic_testChemotaxisNF-kappa Bmedicine.anatomical_structureLiverReceptors Pattern RecognitionModels AnimalCytokinesTumor necrosis factor alphaOriginal Articlemedicine.symptomChemokinesInflammation Mediatorsmedicine.medical_specialtyImmunologyInflammationCCL2Proinflammatory cytokine03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicinePhysical Conditioning AnimalmedicineAnimalsLiver diseasesInflammationbusiness.industryTumor Necrosis Factor-alphaMonocyteBody WeightJNK Mitogen-Activated Protein KinasesCell BiologyLiver Failure Acutemedicine.diseaseEnzyme ActivationMice Inbred C57BL030104 developmental biologyEndocrinologyImmunologybiology.proteinLiver function testsbusinessCell Death & Disease
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