Search results for "Inflammatory cytokine"

showing 10 items of 464 documents

Macrophage-mediated clearance of cells undergoing caspase-3-independent death

2003

Little is known of the functions of caspases in mediating the surface changes required for phagocytosis of dying cells. Here we investigate the role played by the effector caspase, caspase-3 in this process using the caspase-3-defective MCF-7 breast carcinoma line and derived caspase-3-expressing transfectants. Our results indicate that, while certain typical features of apoptosis induced by etoposide - namely classical morphological changes and the ability to degrade DNA into oligonucleosomal fragments - are caspase-3-dependent, loss of cell adhesion to plastic and the capacity to interact with, and to be phagocytosed by, human monocyte-derived macrophages - both by CD14-dependent and CD14…

Programmed cell deathTime FactorsBlotting WesternGreen Fluorescent ProteinsLipopolysaccharide ReceptorsApoptosisCaspase 3PhosphatidylserinesDNA FragmentationTransfectionCaspase 7Proinflammatory cytokinePhagocytosisCell Line TumorSettore BIO/10 - BiochimicaHumansMacrophageAnnexin A5Cell adhesionCytokineMolecular BiologyCells CulturedCaspaseEtoposideCaspase 7InflammationCell DeathbiologyCaspase 3MacrophagesDNACell BiologyCaspaseCell biologyEnzyme ActivationLuminescent ProteinsApoptosisCaspasesbiology.proteinCytokinesElectrophoresis Polyacrylamide GelCell Death & Differentiation
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Glucocorticoids inhibit MAP kinase via increased expression and decreased degradation of MKP-1

2001

Glucocorticoids inhibit the proinflammatory activities of transcription factors such as AP-1 and NF-kappa B as well as that of diverse cellular signaling molecules. One of these signaling molecules is the extracellular signal-regulated kinase (Erk-1/2) that controls the release of allergic mediators and the induction of proinflammatory cytokine gene expression in mast cells. The mechanism of inhibition of Erk-1/2 activity by glucocorticoids is unknown. Here we report a novel dual action of glucocorticoids for this inhibition. Glucocorticoids increase the expression of the MAP kinase phosphatase-1 (MKP-1) gene at the promoter level, and attenuate proteasomal degradation of MKP-1, which we re…

Proteasome Endopeptidase ComplexCell signalingMitogen-Activated Protein Kinase 3Cell Cycle ProteinsBiologyDexamethasoneGene Expression Regulation EnzymologicArticleGeneral Biochemistry Genetics and Molecular BiologyCell LineImmediate-Early ProteinsProinflammatory cytokineMiceGlucocorticoid receptorMultienzyme ComplexesProtein Phosphatase 1Phosphoprotein PhosphatasesAnimalsEnzyme InhibitorsPhosphorylationMolecular BiologyTranscription factorDNA PrimersMitogen-Activated Protein Kinase 1Regulation of gene expressionMitogen-Activated Protein Kinase 3Base SequenceGeneral Immunology and MicrobiologyKinaseHydrolysisGeneral NeuroscienceDual Specificity Phosphatase 1Cell biologyMice Inbred C57BLCysteine EndopeptidasesMitogen-activated protein kinasebiology.proteinMitogen-Activated Protein KinasesProtein Tyrosine PhosphatasesThe EMBO Journal
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Immunomodulating role of bisphosphonates on human gamma delta T cells: an intriguing and promising aspect of their antitumour activity.

2007

Vgamma9Vdelta2 T cells have the ability to produce inflammatory cytokines involved in protective immunity against intracellular pathogens and tumours and to display strong cytolytic as well as bactericidal activities. This suggests a direct involvement of Vgamma9Vdelta2 T lymphocytes in immune control of cancer and infections. These observations have recently aided development of novel immunotherapeutic approaches aimed at Vgamma9Vdelta2 T cell activation. Nitrogen-containing bisphosphonates (N-BPs) play a crucial role in Vgamma9Vdelta2 T lymphocyte activation and in the acquisition of effector functions. The preliminary results of these innovative strategies are encouraging. Moreover, comp…

Protective immunitymedicine.medical_treatmentT cellT-Lymphocytesantitumour bisphophonate human gamma delta T cells immunomodulatory immunotherapyClinical BiochemistryAntineoplastic AgentsBiologyMonocytesProinflammatory cytokineT-Lymphocyte SubsetsNeoplasmsDrug DiscoverymedicineAnimalsHumansImmunologic FactorsPharmacologyDiphosphonatesMechanism (biology)Intracellular parasiteCancerImmunotherapyDendritic Cellsmedicine.diseaseCytolysismedicine.anatomical_structureImmunologyMolecular MedicineInterleukin-2Bone DiseasesExpert opinion on therapeutic targets
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Insights in ChAdOx1 nCoV-19 vaccine-induced immune thrombotic thrombocytopenia

2021

Abstract SARS-CoV-2 vaccine ChAdOx1 nCoV-19 (AstraZeneca) causes a thromboembolic complication termed vaccine-induced immune thrombotic thrombocytopenia (VITT). Using biophysical techniques, mouse models, and analysis of VITT patient samples, we identified determinants of this vaccine-induced adverse reaction. Super-resolution microscopy visualized vaccine components forming antigenic complexes with platelet factor 4 (PF4) on platelet surfaces to which anti-PF4 antibodies obtained from VITT patients bound. PF4/vaccine complex formation was charge-driven and increased by addition of DNA. Proteomics identified substantial amounts of virus production-derived T-REx HEK293 proteins in the ethyle…

ProteomicsAntigen-Antibody ComplexPlatelet Factor 4Extracellular TrapsBiochemistryEpitopesMiceSinus Thrombosis IntracranialMedicinePlateletCell Line TransformedMicroscopybiologyHematologymedicine.anatomical_structureSpike Glycoprotein CoronavirusAntibodyDrug ContaminationVirus CultivationGenetic VectorsImmunologyAdenoviridaeProinflammatory cytokineImaging Three-DimensionalImmune systemAntigenChAdOx1 nCoV-19AnimalsHumansPlatelet activationB cellAutoantibodiesInflammationPurpura Thrombocytopenic IdiopathicSARS-CoV-2business.industryCOVID-19Cell BiologyPlatelet ActivationPlatelets and ThrombopoiesisDynamic Light ScatteringHEK293 CellsImmunoglobulin GImmunologybiology.proteinCapsid ProteinsbusinessCapillary Leak SyndromePlatelet factor 4Extravasation of Diagnostic and Therapeutic MaterialsBlood
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Proteomic Profiling of Secreted Proteins for the Hematopoietic Support of Interleukin-Stimulated Human Umbilical Vein Endothelial Cells

2013

Human umbilical cord vein endothelial cells (HUVECs) secrete a number of factors that greatly impact the proliferation and differentiation of hematopoietic stem and progenitor cells (HSPCs). These factors remain largely unknown. Here, we report on the most comprehensive proteomic profiling of the HUVEC secretome and identified 827 different secreted proteins. Two hundred and thirty-one proteins were found in all conditions, whereas 369 proteins were identified only under proinflammatory conditions following IL-1β, IL-3, and IL-6 stimulation. Thirteen proteins including complement factor b (CFb) were identified only under IL-1β and IL-3 conditions and may potentially represent HSPC prolifer…

ProteomicsSpectrometry Mass Electrospray IonizationInterleukin-1betaBiomedical EngineeringComplement C5blcsh:MedicineAntigens CD34BiologyComplement factor BUmbilical veinProinflammatory cytokineHuman Umbilical Vein Endothelial CellsHumansProgenitor cellCell ProliferationTransplantationInterleukin-6lcsh:RAntibodies MonoclonalComputational BiologyInterleukinComplement System ProteinsCell BiologyFlow CytometryHematopoietic Stem CellsMolecular biologyUp-RegulationComplement systemHaematopoiesisElectrophoresis Polyacrylamide GelInterleukin-3Stem cellPeptidesCell Transplantation
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C7 is expressed on endothelial cells as a trap for the assembling terminal complement complex and may exert anti-inflammatory function.

2009

AbstractWe describe a novel localization of C7 as a membrane-bound molecule on endothelial cells (ECs). Data obtained by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE), Western blot analysis, Northern blot analysis, and mass spectrometry revealed that membrane-associated C7 (mC7) was indistinguishable from soluble C7 and was associated with vimentin on the cell surface. mC7 interacted with the other late complement components to form membrane-bound TCC (mTCC). Unlike the soluble SC5b-9, mTCC failed to stimulate ECs to express adhesion molecules, to secrete IL-8, and to induce albumin leakage through a monolayer of ECs, and more importantly protected ECs from the proinf…

ProteomicsVasculitisUmbilical VeinsVasculitiImmunologyComplementComplement; C7; endothelial cells; inflammationComplement Membrane Attack ComplexBiologyBiochemistryProinflammatory cytokineWestern blotmedicineHumansVimentinC7Interleukin 8Northern blotRNA MessengerMembrane ProteinCells CulturedGel electrophoresisEndothelial Cellmedicine.diagnostic_testCell adhesion moleculeComplement; endothelial cells; inflammationInterleukin-8Endothelial CellsMembrane ProteinsProteomicUmbilical VeinHematologyCell BiologyMolecular biologyComplement C7Endothelial stem cellCells Cultured; Complement C7; Complement Membrane Attack Complex; Endothelial Cells; Humans; Interleukin-8; Membrane Proteins; Proteomics; RNA Messenger; Umbilical Veins; Vasculitis; Vimentin; Hematology; Biochemistry; Cell Biology; Immunologyinflammationendothelial cellComplement membrane attack complexHuman
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Production of reactive oxygen intermediates by human macrophages exposed to soot particles and asbestos fibers and increase in NF-kappa B p50/p105 mR…

1999

Alveolar macrophages (AM) play a decisive role in the immunologic defense system of the lung and in inflammatory pulmonary pathomechanisms. AM and blood monocytes (BM) were exposed to chrysotile B, soot FR 101, and Printex 90 (P 90). We evaluated the reactive oxygen intermediate (ROI) release of AM and BM after particle exposure. ROI release was measured by chemiluminescence. Thirty-minute exposure caused a significant (up to 2.5-fold) increase in ROI release of AM (100 micrograms/10(6) cells) compared with control experiments (p0.01). Identical exposure conditions for BM resulted in a similar reaction pattern (maximum 2.2-fold increase in ROI release; p0.05). After a 90-min particle exposu…

Pulmonary and Respiratory MedicineAdultMaleP50Asbestos Serpentinemedicine.medical_treatmentMonocytesProinflammatory cytokineSuperoxide dismutaseGene expressionMacrophages AlveolarmedicineHumansRNA MessengerReceptorCells CulturedAgedLungbiologyDose-Response Relationship DrugChemistryReverse Transcriptase Polymerase Chain ReactionNF-kappa BMiddle AgedNFKB1Molecular biologyCarbonCytokinemedicine.anatomical_structureGene Expression RegulationImmunologyLuminescent Measurementsbiology.proteinFemaleReactive Oxygen SpeciesBronchoalveolar Lavage FluidLung
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Zur Immunpathogenese des Asthma bronchiale

2000

Allergic asthma is a chronic pulmonary disease associated with bronchoconstriction and inflammation. Recent studies have shown that mediator substances and proinflammatory cytokines produced by mast cells, eosinophils and T-lymphocytes appear to be important for the pathogenesis of asthma. These substances contribute both to the initiation and perpetuation of the disease. In particular, it has been shown that allergic asthma is associated with increased TH2 (IL-4, IL-5, IL-13) cytokine production that causes activation of eosinophils and T-cells and production of chemokines (e.g. eotaxin) by pulmonary fibroblasts. Based on recent advances in our understanding of the immunopathogenesis of as…

Pulmonary and Respiratory MedicineEotaxinChemokinebiologybusiness.industrymedicine.medical_treatmentInflammationImmunoglobulin Emedicine.diseaseProinflammatory cytokineCytokineImmunologybiology.proteinMedicineBronchoconstrictionmedicine.symptombusinessAsthmaPneumologie
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Cigarette smoke exposure inhibits extracellular MMP-2 (gelatinase A) activity in human lung fibroblasts

2007

Abstract Background Exposure to cigarette smoke is considered a major risk factor for the development of lung diseases, since its causative role has been assessed in the induction and maintenance of an inflamed state in the airways. Lung fibroblasts can contribute to these processes, due to their ability to produce proinflammatory chemotactic molecules and extracellular matrix remodelling proteinases. Among proteolytic enzymes, gelatinases A and B have been studied for their role in tissue breakdown and mobilisation of matrix-derived signalling molecules. Multiple reports linked gelatinase deregulation and overexpression to the development of inflammatory chronic lung diseases such as COPD.…

Pulmonary and Respiratory MedicineGelatinase ABiologyMatrix metalloproteinaseProinflammatory cytokineExtracellular matrixExtracellularHumansGelatinaseRNA MessengerLungCells Culturedlcsh:RC705-779Cell DeathPlant ExtractsResearchProteolytic enzymessmoke MMP-2Tissue Inhibitor of MetalloproteinasesEnvironmental Exposurelcsh:Diseases of the respiratory systemEnvironmental exposureFibroblastsrespiratory systemrespiratory tract diseasesCulture Media ConditionedImmunologyMatrix Metalloproteinase 2Tobacco Smoke PollutionEnvironmental MonitoringRespiratory Research
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Mononuclear Cells in Exudative Malignant Pleural Effusions

1994

The aims of this study were to develop a methodology for the isolation of highly enriched mononuclear phagocyte populations from exudative malignant pleural effusions (EMPE) and to characterize the phenotype and functional properties of these cells. Pleural effusion mononuclear cells (PEMC) were isolated by Ficoll centrifugation of EMPE and transudative pleural effusions and allowed to adhere to plastic for 1 h to obtain a pleural effusion mononuclear adherent cell (PEMAC) fraction. Only 66.0±4.2 percent of PEMAC ingested latex particles, indicating that a significant proportion of PEMAC were not phagocytic cells. Latex-positive PEMAC had the morphologic appearance of macrophages and staine…

Pulmonary and Respiratory MedicinePathologymedicine.medical_specialtybusiness.industryPleural effusionCD14InterleukinMononuclear phagocyte systemCritical Care and Intensive Care Medicinemedicine.diseasePeripheral blood mononuclear cellProinflammatory cytokineAntigenMedicineTumor necrosis factor alphaCardiology and Cardiovascular MedicinebusinessChest
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