Search results for "interleukin-1"

showing 10 items of 660 documents

Insulin-like growth factors counteract the effect of interleukin 1 beta on type II phospholipase A2 expression and arachidonic acid release by rabbit…

1994

International audience; Interleukin 1 beta was found to stimulate arachidonic acid release, and the synthesis and secretion of type II phospholipase A2 by rabbit articular chondrocytes in vitro. Interleukin 1 beta had no effect on the level of cytosolic phospholipase A2 mRNA. Insulin-like growth factors, which help stabilize the cartilage matrix, reduced the effect of interleukin 1 beta on type II phospholipase A2 activity and mRNA level, and decreased the Interleukin 1 beta-stimulated arachidonic acid release to the basal values. This suggests that type II phospholipase A2 plays a key role in arachidonic acid release from rabbit articular chondrocytes and that insulin-like growth factors c…

Cartilage Articularmedicine.medical_specialtymedicine.medical_treatmentBiophysicsIn Vitro TechniquesBiochemistryChondrocytePhospholipases AInterleukin 1βInsulin-like growth factorchemistry.chemical_compoundPhospholipase A2[ CHIM.ORGA ] Chemical Sciences/Organic chemistryPhospholipase A2Structural BiologyInsulin-Like Growth Factor IIInternal medicineGeneticsmedicineAnimalsInsulin-like growth factorRNA MessengerInsulin-Like Growth Factor IMolecular BiologyArachidonic Acidbiology[CHIM.ORGA]Chemical Sciences/Organic chemistryArthritisInterleukinCell Biology[CHIM.ORGA] Chemical Sciences/Organic chemistryChondrocyteSomatomedinPhospholipases A2Endocrinologymedicine.anatomical_structureCytokinechemistryInsulin-like growth factor 2biology.proteinArachidonic acidRabbitsInterleukin-1
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Cathepsin B in Antigen-Presenting Cells Controls Mediators of the Th1 Immune Response during Leishmania major Infection

2014

Resistance and susceptibility to Leishmania major infection in the murine model is determined by the capacity of the host to mount either a protective Th1 response or a Th2 response associated with disease progression. Previous reports involving the use of cysteine cathepsin inhibitors indicated that cathepsins B (Ctsb) and L (Ctsl) play important roles in Th1/Th2 polarization during L. major infection in both susceptible and resistant mouse strains. Although it was hypothesized that these effects are a consequence of differential patterns of antigen processing, the mechanisms underlying these differences were not further investigated. Given the pivotal roles that dendritic cells and macrop…

Cathepsin Lmedicine.medical_treatmentCathepsin BCathepsin BWhite Blood CellsMiceAnimal CellsMedicine and Health SciencesLeishmaniasisLeishmania majorProtozoansAntigen PresentationMice Inbred BALB CT CellsAntigen processinglcsh:Public aspects of medicineInterleukin-12Up-RegulationInfectious DiseasesCytokineInterleukin 12FemaleCellular TypesResearch ArticleNeglected Tropical Diseaseslcsh:Arctic medicine. Tropical medicinelcsh:RC955-962Immune CellsImmunologyAntigen presentationAntigen-Presenting CellsMice TransgenicBiologyMajor histocompatibility complexmedicineAnimalsAntigen-presenting cellMHC class IIBlood CellsMacrophagesOrganismsPublic Health Environmental and Occupational HealthBiology and Life Scienceslcsh:RA1-1270Cell BiologyDendritic CellsTh1 CellsTropical DiseasesMolecular biologyParasitic ProtozoansDisease Models AnimalImmunologybiology.proteinPLoS Neglected Tropical Diseases
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Nuclear receptors modulate the interaction of Sp1 and GC-rich DNA via ternary complex formation

2000

Binding sites for transcription factor Sp1have been implicated in the transcriptional regulation of several genes by hormones or vitamins, and here we show that a GC-rich element contributes to the retinoic acid response of the interleukin 1β promoter. To explain such observations, it has been proposed that nuclear receptors can interact with Sp1 bound to GC-rich DNA. However, evidence supporting this model has remained indirect. So far, nuclear receptors have not been detected in a complex with Sp1 and GC-rich DNA, and the expected ternary complexes in non-denaturing gels were not seen. In search for these missing links we found that nuclear receptors [retinoic acid receptor (RAR), thyroid…

Cell ExtractsTranscriptional ActivationReceptors Retinoic AcidSp1 Transcription FactorRecombinant Fusion ProteinsReceptors Cytoplasmic and NuclearTretinoinRetinoic acid receptor betaBiologyRetinoid X receptorLigandsResponse ElementsTransfectionModels BiologicalBiochemistryAntibodiesCell LineSubstrate SpecificityAnimalsPromoter Regions GeneticMolecular BiologyNuclear receptor co-repressor 1Nuclear receptor co-repressor 2Binding SitesReceptors Thyroid HormoneDNACell BiologyRetinoic acid receptor gammaRetinoid X receptor gammaGC Rich SequenceProtein Structure TertiaryNuclear receptor coactivator 1Retinoic acid receptorDrosophila melanogasterEcdysteroneRetinoid X ReceptorsOligodeoxyribonucleotidesBiochemistryReceptors CalcitriolThermodynamicsResearch ArticleInterleukin-1Protein BindingTranscription FactorsBiochemical Journal
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Indicaxanthin inhibits NADPH oxidase (NOX)-1 activation and NF-κB-dependent release of inflammatory mediators and prevents the increase of epithelial…

2014

Dietary redox-active/antioxidant phytochemicals may help control or mitigate the inflammatory response in chronic inflammatory bowel disease (IBD). In the present study, the anti-inflammatory activity of indicaxanthin (Ind), a pigment from the edible fruit of cactus pear (Opuntia ficus-indica, L.), was shown in an IBD model consisting of a human intestinal epithelial cell line (Caco-2 cells) stimulated by IL-1β, a cytokine known to play a major role in the initiation and amplification of inflammatory activity in IBD. The exposure of Caco-2 cells to IL-1β brought about the activation of NADPH oxidase (NOX-1) and the generation of reactive oxygen species (ROS) to activate intracellular signal…

Cell Membrane PermeabilityPyridinesPyridinemedicine.medical_treatmentInterleukin-1betaMedicine (miscellaneous)Nitric Oxide Synthase Type IIIndicaxanthinNADPH OxidaseInflammatory bowel diseaseIntestinal absorptionAntioxidantschemistry.chemical_compoundSettore BIO/10 - BiochimicaInflammation MediatorCaco-2 CellNutrition and DieteticsNADPH oxidasebiologyNF-kappa BNADPH Oxidase 1OpuntiaCell biologyBetaxanthinsCytokineNADPH Oxidase 1EnterocyteAntioxidantmedicine.symptomInflammation MediatorsReactive Oxygen SpecieIndicaxanthinHumanRedox-active phytochemicalInflammationIn vitro modelmedicineHumansIndicaxanthin Betalain pigments Inflammatory bowel disease Redox-active phytochemicalsInterleukin 8Inflammationbusiness.industryInterleukin-6Interleukin-8NADPH OxidasesInflammatory Bowel DiseasesEnzyme ActivationEnterocyteschemistryIntestinal AbsorptionCaco-2Cyclooxygenase 2BetaxanthinFruitImmunologybiology.proteinCaco-2 CellsbusinessReactive Oxygen SpeciesThe British journal of nutrition
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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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Induction of programmed cell death in human retinoblastoma Y79 cells by C2-ceramide.

1998

C2-ceramide, a cell-permeable analogue of ceramide, induced significant, dose- and time-dependent death in human retinoblastoma Y79 cells. Dying cells strongly displayed the morphology of apoptosis as characterized by microscopic evidence of cell shrinkage, membrane blebbing, nuclear and chromatin condensation and degeneration of the nucleus into membrane-bound apoptotic bodies. Upon induction of apoptosis Y79 cells evidence early phosphatidylserine externalization, as shown by annexin V-FITC. Apoptosis was also assessed by monitoring changes in cell granularity by staining with the combined fluorescent dyes acridine orange and ethidium bromide. C2-ceramide induced these morphological chang…

Cell SurvivalBlotting WesternRetinoblastomaProteinsApoptosisDNA FragmentationCeramidesC2-ceramideNucleosomesSphingomyelin PhosphodiesteraseBacterial ProteinsProto-Oncogene Proteins c-bcl-2SphingosineOkadaic AcidTumor Cells CulturedHumansTumor Suppressor Protein p53Interleukin-1Molecular and cellular biochemistry
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NKG2D induces Mcl-1 expression and mediates survival of CD8 memory T cell precursors via phosphatidylinositol 3-kinase.

2013

Abstract Memory formation of activated CD8 T cells is the result of a specific combination of signals that promote long-term survival and inhibit differentiation into effector cells. Much is known about initial cues that drive memory formation, but it is poorly understood which signals are essential during the intermediate stages before terminal differentiation. NKG2D is an activating coreceptor on Ag-experienced CD8 T cells that promotes effector cell functions. Its role in memory formation is currently unknown. In this study, we show that NKG2D controls formation of CD8 memory T cells by promoting survival of precursor cells. We demonstrate that NKG2D enhances IL-15–mediated PI3K signalin…

Cell SurvivalImmunologyCytomegalovirusBiologyCD8-Positive T-LymphocytesLymphocyte ActivationMiceMemory cellPrecursor cellmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorReceptors ImmunologicInterleukin-15Mice KnockoutPrecursor Cells T-LymphoidNK cells; NKG2D; CD8 T cellsEffectorCell DifferentiationNKG2DNKG2D; CD8 T cell memory; Mcl1; PI3KCell biologyMice Inbred C57BLmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2NK Cell Lectin-Like Receptor Subfamily KCytomegalovirus InfectionsMyeloid Cell Leukemia Sequence 1 ProteinPhosphatidylinositol 3-KinaseMemory T cellImmunologic MemoryCD8Signal TransductionJournal of immunology (Baltimore, Md. : 1950)
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Anti-inflammatory effects of chemically modified tetracyclines by the inhibition of nitric oxide and interleukin-12 synthesis in J774 cell line

2001

We investigated the effects of chemically modified tetracyclines (CMTs) on the production of nitric oxide (NO) and on the synthesis of some cytokines: tumour necrosis factor alpha (TNF-alpha), interleukin(IL)-10 and IL-12 in lipopolysaccharide (LPS)-treated J774 cell line. Furthermore, we studied the ability of these drugs to modify the viability in LPS-stimulated J774 macrophages. CMTs decreased, in a dose-dependent manner, inducible NO synthase (iNOS) activity and, consequently, nitrite formation in J774 cultures. The CMT-induced decrease in NO production is due to the inhibition of enzyme activity rather than to a direct effect on enzyme expression. The absence of the inhibition in mRNA …

Cell Survivalmedicine.medical_treatmentImmunologyNitric Oxide Synthase Type IIApoptosisEnzyme-Linked Immunosorbent AssayNitric OxideCell LineNitric oxideMicechemistry.chemical_compoundEthidiumIn Situ Nick-End LabelingmedicineAnimalsImmunology and AllergyRNA MessengerViability assayEnzyme InhibitorsFluorescent DyesPharmacologybiologyReverse Transcriptase Polymerase Chain ReactionAnti-Inflammatory Agents Non-SteroidalInterleukinBiological activityInterleukin-12Acridine OrangeCell biologyNitric oxide synthaseInterleukin 10CytokinechemistryBiochemistryTetracyclinesApoptosisbiology.proteinCytokinesElectrophoresis Polyacrylamide GelIndicators and ReagentsNitric Oxide SynthaseInternational Immunopharmacology
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Interleukin-10-treated dendritic cells do not inhibit Th2 immune responses in ovalbumin/alum-sensitized mice.

2005

<i>Background:</i> It is well known that the immunoregulatory cytokine interleukin (IL)-10 inhibits the accessory function of human dendritic cells (DC) in vitro. Recently, we have shown that these IL-10 DC inhibit the production of T helper cell 1 (Th1) and T helper cell 2 (Th2) cytokines by T cells from atopic individuals in vitro. The current study was set out to analyze whether IL-10 DC also exert inhibitory effects in vivo in a murine model of allergy to ovalbumin adsorbed to the adjuvant aluminium hydroxide (OVA/alum). <i>Methods:</i> OVA-pulsed or unpulsed bone marrow-derived DC, treated with IL-10 or left untreated during generation, were injected intravenous…

Cell TransplantationOvalbuminmedicine.medical_treatmentImmunologyLymphocyte ActivationMiceImmune systemTh2 CellsAdjuvants ImmunologicmedicineHypersensitivityImmune ToleranceImmunology and AllergyAnimalsAntigen-presenting cellCell ProliferationMice Inbred BALB CbiologyInterleukinGeneral MedicineDendritic cellDendritic CellsImmunoglobulin EFlow CytometryInterleukin-10OvalbuminInterleukin 10Disease Models AnimalCytokineImmunologybiology.proteinInterleukin 12Alum CompoundsCytokinesFemaleInternational archives of allergy and immunology
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