Search results for "macrophage"

showing 10 items of 781 documents

Activation of complement by the alternative pathway as a factor in the pathogenesis of periodontal disease.

1976

Dental plaque and a bacterium, Actinomyces viscosus, isolated from plaque that can reproduce periodontal disease in germ-free rats, are activators of complement by the alternative pathway. It is suggested that this process is involved in the pathogenesis of chronic inflammatory periodontal disease.

T-LymphocytesGuinea PigsDental PlaqueAntigen-Antibody ComplexDental plaquePathogenesisstomatognathic systemPeriodontal diseasemedicineActinomycesAnimalsHumansActinomyces viscosusBone ResorptionPeriodontitisGlycoproteinsB-LymphocytesEnzyme Precursorsbusiness.industryMacrophagesGlobulinsGeneral MedicineComplement C3Complement System Proteinsmedicine.diseaseCathepsinsComplement (complexity)RatsEndotoxinsstomatognathic diseasesMicrobial CollagenaseImmunologyAlternative complement pathwaybusinessLancet (London, England)
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cIAP1-dependent TRAF2 degradation regulates the differentiation of monocytes into macrophages and their response to CD40 ligand.

2008

AbstractPeripheral blood monocytes are plastic cells that migrate to tissues and differentiate into various cell types, including macrophages, dendritic cells, and osteoclasts. We have described the migration of cellular inhibitor of apoptosis protein 1 (cIAP1), a member of the IAP family of proteins, from the nucleus to the Golgi apparatus in monocytes undergoing differentiation into macrophages. Here we show that, once in the cytoplasm, cIAP1 is involved in the degradation of the adaptor protein tumor necrosis factor receptor–associated factor 2 (TRAF2) by the proteosomal machinery. Inhibition of cIAP1 prevents the decrease in TRAF2 expression that characterizes macrophage formation. We d…

TRAF2CytoplasmCellular differentiationImmunologyCD40 LigandDown-RegulationGene ExpressionGolgi ApparatusBiologyBiochemistryMonocytesProinflammatory cytokineInhibitor of Apoptosis ProteinsPhagocytes Granulocytes and MyelopoiesisPhagocytosisMacrophageHumansRNA Small InterferingCD40U937 cellMacrophagesSignal transducing adaptor proteinCell DifferentiationCell BiologyHematologyU937 CellsTNF Receptor-Associated Factor 2Molecular biologyCell biologybiology.proteinTumor necrosis factor alphaBlood
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Taurine chloramine inhibits functional responses of human eosinophils in vitro

2009

10 páginas, 7 figuras, 1 tabla.

Taurinemedicine.medical_specialtyTaurineImmunologyApoptosisEosinophil peroxidasechemistry.chemical_compoundSuperoxidesInternal medicineTaurine-chloraminemedicineHumansImmunology and AllergyEnzyme InhibitorsSuperoxide anionCells CulturedPeroxidaseRespiratory BurstEosinophil cationic proteinbiologySuperoxideEosinophil Cationic ProteinZymosanNF-kappa BGranulocyte-Macrophage Colony-Stimulating FactorNADPH OxidasesEosinophilPhosphoproteinsMolecular biologyHuman eosinophilsLeukotriene C4Respiratory burstEosinophilsmedicine.anatomical_structureEndocrinologychemistryEicosanoidbiology.proteinCalciumEosinophil cationic proteinInterleukin-5Eosinophil peroxidase
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LAAE-14, a new in vitro inhibitor of intracellular calcium mobilization, modulates acute and chronic inflammation.

2003

Abstract A new lipidic acid-amido ether derivative (LAAE-14) able to reduce dose-dependently the calcium increases mediated either by calcium ionophore ionomycin, by the endoplasmic reticular Ca 2+ -ATPase inhibitor thapsigargin, or by the chemotactic tripeptide N -formyl- l -methionyl- l -leucyl- l -phenylalanine (fMLP), in human neutrophils as well as in murine peritoneal macrophages, but not ATP, has been evaluated as a potential anti-inflammatory drug. This compound attenuated leukocyte activation by means of its inhibitory effect on the respiratory burst elicited in both types of cells by 12- O -tetradecanoyl phorbol 13-acetate, by inhibition of the degranulation process induced by cyt…

ThapsigarginNeutrophilschemistry.chemical_elementCalciumPharmacologyCarrageenanBiochemistryLeukotriene B4Calcium in biologyDinoprostonechemistry.chemical_compoundMiceCell MovementAnimalsEdemaHumansCytochalasin BNitritesPharmacologyInflammationPlatelet-activating factorPancreatic ElastaseTumor Necrosis Factor-alphaZymosanArthritis ExperimentalRatsDisease Models AnimalchemistryBiochemistryIonomycinAcute DiseaseChronic DiseaseLuminescent MeasurementsPhorbolMacrophages PeritonealTumor necrosis factor alphaCalciumBiochemical pharmacology
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Inhibition of in vitro macrophage-induced low density lipoprotein oxidation by thyroid compounds

2003

Oxidized low density lipoproteins (LDL) are highly suspected of initiating the atherosclerosis process. Thyroid hormones and structural analogues have been reported to protect LDL from lipid peroxidation induced by Cu2+ or the free radical generator 2,2'-azobis-'2-amidinopropane' dihydrochloride in vitro. We have examined the effects of thyroid compounds on macrophage-induced LDL oxidation. Human monocyte-derived macrophages (differentiated U937 cells) were incubated for 24 h with LDL and different concentrations (0-20 microM) of 3,5,3'-triiodo-l -thyronine (T3), 3,5,3',5'-tetraiodo-L-thyronine (T4), 3,3',5'-tri-iodo-l -thyronine (rT3), the T3 acetic derivative (3,5,3'-tri-iodothyroacetic a…

Thyroid Hormonesmedicine.medical_specialtyMacrophagesEndocrinology Diabetes and MetabolismU937 CellsThiobarbituric Acid Reactive SubstancesRedoxIn vitroLipoproteins LDLLipid peroxidationchemistry.chemical_compoundEndocrinologyEndocrinologychemistryIn vivoLow-density lipoproteinInternal medicineTBARSmedicineHumansLipid PeroxidationViability assayIntracellularJournal of Endocrinology
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T-cell-mediated cytotoxicity against herpes simplex virus-infected target cells

1977

THE control of herpes simplex virus (HSV) infection by immunological mechanisms seems to be complex and is poorly understood. Neutralising antibodies to HSV plus complement seem to have no effect on the propagation of HSV infection, because HSV spreads to adjacent cells by passing through intercellular bridges1–3. Anti-HSV antibodies plus complement, however, destroy virus-infected cells, but cannot prevent the spread of HSV, suggesting that the virus must be transferred to neighbouring cells before immune lysis occurs1,5. Therefore if lymphocyte-mediated cytolytic mechanisms are instrumental in blocking the spread of HSV in vivo, they ought to destroy infected cells at a very early stage i…

Time FactorsCell SurvivalT-Lymphocytesvirusesmedicine.disease_causeVirusMicrobiologyMiceImmune systemmedicineAnimalsSimplexvirusCytotoxic T cellCells CulturedAntibody-dependent cell-mediated cytotoxicityMultidisciplinarybiologyMacrophagesHerpes SimplexCytotoxicity Tests ImmunologicVirologyCTL*Herpes simplex virusMice Inbred CBAbiology.proteinAntibodyT cell mediated cytotoxicityNature
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Characterization of lymphokine-mediated activation of macrophages for antigen presentation: studies with long-term cultured bone marrow-derived macro…

1984

In cultures of bone marrow (BM) supplemented with L cell-derived colony-stimulating factor a pure population of macrophages (M phi) differentiates, which can be further propagated with a doubling time of 3.8 days. "Young" BMM phi obtained on day 8 of culture were shown to act as antigen-presenting cells inducing the antigen-specific proliferation of the cloned T cell line ST2/K.9, whereas "old" M phi had lost this ability. However, at any time tested (up to 132 days) the presentation function of old BMM phi could be completely restored by pulsing the cells with lymphokines (LK). A duration of 11 hr for the LK-pulse was sufficient to trigger the M phi to exert an optimal presentation functio…

Time FactorsT cellT-LymphocytesImmunologyPopulationAntigen presentationAntigen-Presenting CellsBone Marrow CellsBiologyLymphocyte ActivationInterferon-gammaMiceImmune systemAntigenmedicineImmunology and AllergyDoubling timeAnimalseducationCells Culturededucation.field_of_studyLymphokinesLymphokineHematologyMacrophage ActivationMolecular biologymedicine.anatomical_structureImmunologyBone marrowImmunobiology
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Prostaglandin E(2)-loaded microspheres as strategy to inhibit phagocytosis and modulate inflammatory mediators release.

2008

PGE(2), an arachidonic acid metabolite produced by various type of cells regulates a broad range of physiological activities in the endocrine, cardiovascular, gastrointestinal, and immune systems, and is involved in maintaining the local homeostasis. In the immune system, PGE(2) is mainly produced by APCs and it can suppress the Th1-mediated immune responses. The aim of this study was to develop PGE(2)-loaded biodegradable MS that prolong and sustain the in vivo release of this mediator. An o/w emulsion solvent extraction-evaporation method was chosen to prepare the MS. We determined their diameters, evaluated the in vitro release of PGE(2), using enzyme immunoassay and MS uptake by periton…

Time Factorsmedicine.medical_treatmentPhagocytosisChemistry PharmaceuticalDrug CompoundingPharmaceutical ScienceInflammationPharmacologyBiologyNitric OxideDinoprostonechemistry.chemical_compoundMiceImmune systemPhagocytosisIn vivoSepsismedicineAnimalsHumansImmunologic FactorsProstaglandin E2Particle SizeCells CulturedChemokine CCL2Tumor Necrosis Factor-alphaEndothelial CellsWaterGeneral MedicineMicrospheresDisease Models AnimalchemistryBiochemistrySolubilityDelayed-Action PreparationsMacrophages PeritonealLiberationlipids (amino acids peptides and proteins)Arachidonic acidEmulsionsmedicine.symptomInflammation MediatorsOilsBiotechnologyProstaglandin Emedicine.drugEuropean journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V
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Urokinase activates macrophage PON2 gene transcription via the PI3K/ROS/MEK/SREBP-2 signalling cascade mediated by the PDGFR-β

2009

Aims We have recently shown that urokinase plasminogen activator (uPA) increases oxidative stress (OS), cholesterol biosynthesis, and paraoxonase 2 (PON2) expression in macrophages via binding to its receptor, the uPAR. Since PON2 is regulated by both OS and cholesterol content, we hypothesized that uPA elicits a cascade of signal transduction events shared by NADPH oxidase and cholesterol biosynthesis that culminates in PON2 gene expression. Here, we investigated the signalling pathway that leads to the expression of PON2 in macrophages in response to uPA. Methods and results The increase in macrophage PON2 mRNA levels in response to uPA was shown to depend on PON2 gene promoter activation…

Transcription GeneticPhysiologyReceptor Platelet-Derived Growth Factor betaPhosphatidylinositol 3-KinasesPhysiology (medical)Gene expressionHumansExtracellular Signal-Regulated MAP KinasesTranscription factorCells CulturedMitogen-Activated Protein Kinase KinasesRegulation of gene expressionNADPH oxidasebiologyAryldialkylphosphataseKinaseMacrophagesNADPH OxidasesUrokinase-Type Plasminogen ActivatorCell biologySterol regulatory element-binding proteinUrokinase receptorGene Expression RegulationBiochemistryTissue Plasminogen Activatorbiology.proteinSignal transductionReactive Oxygen SpeciesCardiology and Cardiovascular MedicineSignal TransductionSterol Regulatory Element Binding Protein 2Cardiovascular Research
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Interleukin-4 induces secretion of CSF for granulocytes and CSF for macrophages by peripheral blood monocytes.

1989

Abstract T cells are known to interact cooperatively with monocytes to produce Colony-Stimulating Factors (CSF), although T cell-mediated signals leading to CSF secretion by monocytes are not completely understood. We have made use of Northern blot hybridization and specific bioassays to study the effects of the T cell product interleukin-4 (IL-4) on monocyte CSF expression. The results suggest a previously unrecognized role of IL-4 as a CSF inducer since exposure of monocytes to IL-4 resulted in accumulation of transcripts for granulocyte-CSF (G-CSF) and macrophage-CSF (M-CSF). Consequently, IL-4-activated monocytes released factors in their culture supernatants biologically and antigenica…

Transcription GeneticT cellImmunologyBiologyBiochemistryMonocytesColony-Forming Units AssayMiceColony-Stimulating FactorsGranulocyte Colony-Stimulating FactormedicineBioassayAnimalsHumansInducerSecretionNorthern blotInterleukin 4Mice Inbred C3HMonocyteInterleukinsMacrophage Colony-Stimulating FactorMacrophagesCell BiologyHematologyMolecular biologyPeripheral bloodRecombinant Proteinsmedicine.anatomical_structureImmunologyInterleukin-4GranulocytesBlood
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