Search results for "Monocytes"

showing 10 items of 286 documents

Association between COX-2 rs 6681231 genotype and interleukin-6 in periodontal connective tissue. A pilot study.

2014

[Objectives] The aim of this pilot study was to investigate associations between IL-6 and COX-2 expression in gingival biopsies and both clinical diagnosis and genotypes in the IL-6 and COX-2 genes. [Design] A case-control study included 41 gingival biopsies obtained from Caucasian patients grouped according to clinical diagnosis of gingival health (n = 10), gingivitis (n = 15) or chronic periodontitis (n = 16). Immunohistochemistry analyses were performed to determine COX-2 expression in lamina propria, IL-6 expression in lamina propria and gingival epithelium and level of inflammatory cell infiltrate. Individual DNA was extracted and genotyped by real-time PCR for IL6 SNPs rs 2069827 and …

Bacterial DiseasesMaleBiopsyGingivaDentistryGene ExpressionPilot ProjectsEpitheliumMonocytesGingivitisGenotypehealth care economics and organizationsPlasma cellsMultidisciplinaryGingival AbscessesbiologyQRMiddle AgedGingivitishumanitiesmedicine.anatomical_structureInfectious DiseasesCOX-2 6681231 genotype interleukin-6 periodontitisCytokinesPeriodontal AbscessesMedicineFemalemedicine.symptomPeriodontal IndexConnective tissueImmunohistochemical AnalysisResearch ArticleAdultmedicine.medical_specialtyClinical Research DesignScienceOral MedicineConnective tissueHemorrhagePolymorphism Single NucleotideInternal medicinemedicineGeneticsHumansInterleukin 6PeriodontitisBiologyAgedPeriodontitisClinical GeneticsInflammationbusiness.industryInterleukin-6Case-control studymedicine.diseaseChronic periodontitisHaplotypesCyclooxygenase 2Immune SystemCase-Control StudiesChronic Periodontitisbiology.proteinGenetic PolymorphismImmunologic TechniquesClinical ImmunologybusinessPopulation GeneticsPLoS ONE
researchProduct

Characterization of cells involved in the formation of granuloma. An ultrastructural study on macrophages, epitheloid cells, and giant cells in exper…

1981

In experimental tubulo-interstitial (anti-basement membrane) nephritis of the rat, granulomatous inflammation develops around immunologically altered tubular basement membranes. The present light- and electron microscopic studies indicate that in the course of the granulomatous reaction, tissue monocytes evolve from blood monocytes and pursue two independent pathways of differentation. On the one hand they may differentiate into macrophages ("distant from tubules") or, alternatively, into epitheloid cells ("adjacent to tubules"). The latter, through cell fusion, develop into multinucleated giant cells of the Langhans' type. The cytoplasmic components of the epitheloid cells and the multinuc…

Basement membraneMaleCell fusionGranulomaInterstitial nephritisMacrophagesLanghans giant cellGeneral MedicineBiologymedicine.diseaseBasement MembraneMonocytesCell biologyRatsCell FusionMicroscopy Electronmedicine.anatomical_structureKidney TubulesGiant cellGranulomamedicineUltrastructureAnimalsNephritis InterstitialNephritisVirchows Archiv. B, Cell pathology including molecular pathology
researchProduct

Vitamin C blocks inflammatory platelet-activating factor mimetics created by cigarette smoking.

1997

Cigarette smoking within minutes induces leukocyte adhesion to the vascular wall and formation of intravascular leukocyte-platelet aggregates. We find this is inhibited by platelet-activating factor (PAF) receptor antagonists, and correlates with the accumulation of PAF-like mediators in the blood of cigarette smoke-exposed hamsters. These mediators were PAF-like lipids, formed by nonenzymatic oxidative modification of existing phospholipids, that were distinct from biosynthetic PAF. These PAF-like lipids induced isolated human monocytes and platelets to aggregate, which greatly increased their secretion of IL-8 and macrophage inflammatory protein-1alpha. Both events were blocked by a PAF r…

Blood PlateletsChemokineAntioxidantTime FactorsPlatelet Aggregationmedicine.drug_classNeutrophilsmedicine.medical_treatmentPhospholipidReceptors Cell SurfaceAscorbic AcidPlatelet Membrane GlycoproteinsPharmacologyAntioxidantsMonocytesReceptors G-Protein-Coupledchemistry.chemical_compoundReference ValuesCricetinaemedicineCell AdhesionAnimalsHumansPlateletPlatelet Activating FactorReceptorChemokine CCL4Cell AggregationLeukocyte aggregationbiologyPlatelet-activating factorChemistryInterleukin-8SmokingGeneral MedicineAzepinesMacrophage Inflammatory ProteinsTriazolesReceptor antagonistBiochemistrybiology.proteinlipids (amino acids peptides and proteins)Platelet Aggregation InhibitorsResearch Article
researchProduct

Leukocyte–platelet aggregates—a phenotypic characterization of different stages of peripheral arterial disease

2016

The formation of monocyte-platelet aggregates and neutrophil-platelet aggregates (MPA and NPA, respectively) is influenced by inflammation, but also might contribute to an exacerbation of inflammatory responses in atherosclerotic plaque. The purpose of this study was to analyze MPA and NPA proportions in regard to different stages of peripheral arterial disease (PAD). Forty-five patients with intermittent claudication (IC) (3 groups: Rutherford (R)-1, R-2, and R-3; each n = 15), 20 patients with critical limb ischemia (CLI) (Rutherford 5 (40%) and 6 (60%)), and 20 healthy controls were studied. Analyses of monocyte (Mon) subpopulations (CD14++CD16- (classical) Mon1, CD14++CD16+ (intermediat…

Blood PlateletsMale0301 basic medicinemedicine.medical_specialtyNeutrophilsLipopolysaccharide ReceptorsInflammationComorbidity030204 cardiovascular system & hematologyFibrinogenMonocytesProinflammatory cytokinePeripheral Arterial Disease03 medical and health sciences0302 clinical medicineRisk FactorsInternal medicineLeukocytesmedicineHumansPlateletReceptors ImmunologicAgedCell AggregationWhole bloodAged 80 and overbusiness.industryMonocyteReceptors IgGHematologyGeneral MedicineCritical limb ischemiaMiddle AgedFlow CytometryIntermittent claudicationBlood Cell CountPhenotype030104 developmental biologyEndocrinologymedicine.anatomical_structureImmunologyFemalemedicine.symptombusinessCell Adhesion MoleculesBiomarkersmedicine.drugPlatelets
researchProduct

Cyclooxygenase-1/2 (COX-1/COX-2) and 5-lipoxygenase (5-LOX) inhibitors of the 6,7-diaryl-2,3-1H-dihydropyrrolizine type

2003

A series of 6,7-diaryl-2,3-1H-dihydropyrrolizines was prepared as COX-1/COX-2 and 5-LOX inhibitors. The inhibition of COX-1 was evaluated using intact bovine platelets as the enzyme source, whereas LPS-stimulated human monocytes served as the enzyme source for inducible COX-2. The determination of arachidonic metabolites was performed by HPLC for COX-1 and RIA for COX-2. The balance between COX-1/COX-2 and 5-LOX inhibition can be shifted by modifying the substitution pattern of the phenyl moiety at the 6- and 7-position of the pyrrolizine nucleus. Structure-activity relationships are discussed.

Blood PlateletsRadioimmunoassayHigh-performance liquid chromatographyIsozymeMonocytesDrug DiscoverymedicineCox 1 cox 2AnimalsHumansMoietyStructure–activity relationshipPyrrolesPlateletLipoxygenase InhibitorsEnzyme InhibitorsChromatography High Pressure LiquidPharmacologychemistry.chemical_classificationbiologyChemistryOrganic ChemistryMembrane ProteinsGeneral MedicineIn vitroIsoenzymesmedicine.anatomical_structureEnzymeBiochemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesEnzyme inhibitorDrug DesignArachidonate 5-lipoxygenaseCyclooxygenase 1biology.proteinCattleCyclooxygenaseNucleusEuropean Journal of Medicinal Chemistry
researchProduct

IL-27 improves migrational and antiviral potential of CB dendritic cells.

2013

Abstract Interleukin (IL)-27 is known to be increased considerably in cord blood (CB) dendritic cells (DCs) after TLR ligation. Previously, we demonstrated that also basal IL-27 levels are higher in CB DCs. Here, we examined effects of IL-27 on monocyte derived dendritic cells (moDCs) to approach its particular role in the specialized immune system of the human neonate. Exogenous IL-27 promotes IL-27 transcription in CB and adult blood (AB) moDCs. IL-27 acts on CB moDCs primarily by significantly augmenting IL-27 protein, secondarily by increasing transcription of CXCL10 among other chemokines, chemokine receptor CCR1, interferon stimulated genes, transcription factor IRF8 and genes involve…

CCR1AdultChemokineTranscription GeneticImmunologyAntigen presentationReceptors CCR1MonocytesChemokine receptorInterferonCell MovementmedicineImmunology and AllergyCXCL10HumansCells CulturedbiologyTumor Necrosis Factor-alphaInterleukinsInterleukin-8Infant NewbornInterleukinCell DifferentiationGeneral MedicineDendritic CellsFetal BloodChemokine CXCL10STAT1 Transcription FactorGene Expression RegulationInterferon Regulatory Factorsbiology.proteinCancer researchIRF8medicine.drugSignal TransductionHuman immunology
researchProduct

The Cytokine GM-CSF Drives the Inflammatory Signature of CCR2+ Monocytes and Licenses Autoimmunity.

2015

Granulocyte-macrophage colony-stimulating factor (GM-CSF) has emerged as a crucial cytokine produced by auto-reactive T helper (Th) cells that initiate tissue inflammation. Multiple cell types can sense GM-CSF, but the identity of the pathogenic GM-CSF-responsive cells is unclear. By using conditional gene targeting, we systematically deleted the GM-CSF receptor (Csf2rb) in specific subpopulations throughout the myeloid lineages. Experimental autoimmune encephalomyelitis (EAE) progressed normally when either classical dendritic cells (cDCs) or neutrophils lacked GM-CSF responsiveness. The development of tissue-invading monocyte-derived dendritic cells (moDCs) was also unperturbed upon Csf2r…

CCR2Myeloidmedicine.medical_treatmentInterleukin-1betaAutoimmunitymedicine.disease_causeMonocytesAutoimmunityCytokine Receptor Common beta Subunit0302 clinical medicineSTAT5 Transcription FactorImmunology and AllergyAntigens LyMyeloid CellsPhosphorylationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionExperimental autoimmune encephalomyelitisGene targetingFlow CytometryInfectious DiseasesCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factor2723 Immunology and Allergymedicine.symptommedicine.drugSignal TransductionEncephalomyelitis Autoimmune ExperimentalReceptors CCR2Immunology610 Medicine & healthInflammationMice TransgenicBiology03 medical and health sciencesmedicineAnimalsHumans030304 developmental biologyInflammation2403 ImmunologyGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesDendritic Cellsmedicine.disease10040 Clinic for NeurologyImmunologyTranscriptome030217 neurology & neurosurgery
researchProduct

Regulation of IL-12 p40 Promoter Activity in Primary Human Monocytes: Roles of NF-κB, CCAAT/Enhancer-Binding Protein β, and PU.1 and Identification o…

2001

Abstract Appropriate regulation of IL-12 expression is critical for cell-mediated immune responses. In the present study, we have analyzed the regulation of IL-12 p40 promoter activity in primary human monocytes in vivo. Accordingly, we analyzed the p40 promoter by in vivo footprinting in resting and activated primary human blood CD14+ monocytes. Interestingly, footprints at binding sites for trans-activating proteins such as C/EBP, NF-κB, and ETS were only found upon stimulation with LPS and IFN-γ. In contrast, a footprint over a purine-rich sequence at −155, termed GA-12 (GATA sequence in the IL-12 promoter), was observed in resting, but not activated, cells. Further characterization of t…

CD14ImmunologyDNA FootprintingLipopolysaccharide ReceptorsRepressorBiologyDinoprostoneMonocytesCell LineMicechemistry.chemical_compoundProto-Oncogene ProteinsGene expressionAnimalsHumansImmunology and AllergyBinding sitePromoter Regions GeneticPsychological repressionCells CulturedDNA PrimersBase SequenceCcaat-enhancer-binding proteinsCCAAT-Enhancer-Binding Protein-betaBinding proteinNF-kappa BNuclear ProteinsNF-κBInterleukin-12Molecular biologychemistryMutagenesis Site-DirectedTrans-ActivatorsInterleukin-4The Journal of Immunology
researchProduct

Flow cytometry and spectral imaging multiphoton microscopy analysis of CD36 expression with quantum dots 605 of untreated and 7-ketocholesterol-treat…

2006

To evaluate CD36 expression with quantum dots 605 (QDs 605) on untreated and 7-ketocholesterol (7KC)-treated monocytic U937 cells by flow cytometry (FCM) and confocal and multiphoton laser scanning microscopy (CLSM).Cells were analyzed by CLSM, following flow cytometric quantification of CD36 expression and 7KC uptake. Image sequences were obtained by spectral analysis in monophoton and multiphoton CLSM and analyzed by the factor analysis of medical image sequences (FAMIS) algorithm to differentiate emission spectra. In CLSM analysis, cell deposits were screened in ultraviolet excitation modes to optimize the possibilities of QDs 605 and have the benefit of nuclei counterstaining by DAPI.FC…

CD36 AntigensMESH: PhotonsMESH : Flow CytometryMESH: AlgorithmsMESH: Flow CytometryMESH: U937 CellsMESH : Quantum DotsMESH: MonocytesMonocytesMESH : Microscopy Fluorescence MultiphotonMESH : PhotonsQuantum DotsMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyKetocholesterols[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCells CulturedMESH : AlgorithmsMESH : KetocholesterolsPhotonsMESH: HumansMESH: Antigens CD36MESH : HumansMESH: KetocholesterolsU937 CellsMESH: Quantum DotsFlow CytometryMESH : Antigens CD36Microscopy Fluorescence MultiphotonMESH : MonocytesMESH : U937 CellsMESH: Microscopy Fluorescence MultiphotonAlgorithmsMESH: Cells Cultured
researchProduct

Induction of CD36 and thrombospondin-1 in macrophages by hypoxia-inducible factor 1 and its relevance in the inflammatory process.

2012

Inflammation is part of a complex biological response of vascular tissue to pathogens or damaged cells. First inflammatory cells attempt to remove the injurious stimuli and this is followed by a healing process mediated principally by phagocytosis of senescent cells. Hypoxia and p38-MAPK are associated with inflammation, and hypoxia inducible factor 1 (HIF-1) has been detected in inflamed tissues. We aimed to analyse the role of p38-MAPK and HIF-1 in the transcriptional regulation of CD36, a class B scavenger receptor, and its ligand thrombospondin (TSP-1) in macrophages and to evaluate the involvement of this pathway in phagocytosis of apoptotic neutrophils. We have also assessed HIF-1α, p…

CD36 AntigensMaleAnatomy and PhysiologyNeutrophilsCD36Digestive Physiologylcsh:MedicineApoptosisp38 Mitogen-Activated Protein KinasesBiochemistryMonocytesThrombospondin 1Intestinal mucosaCrohn DiseaseIntestinal Mucosalcsh:ScienceHypoxiaPromoter Regions GeneticMultidisciplinaryProtein StabilityMiddle AgedOxygen Metabolismmedicine.anatomical_structureMedicineFemaleHypoxia-Inducible Factor 1medicine.symptomProtein BindingSignal TransductionResearch ArticleAdultCell PhysiologyAdolescentPhagocytosisImmune CellsImmunologyInflammationGastroenterology and HepatologyBiologyCell LineYoung AdultPhagocytosismedicineHumansUlcerative ColitisScavenger receptorBiologyInflammationLamina propriaDigestive RegulationMacrophageslcsh:RInflammatory Bowel DiseaseHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitMetabolismApoptosisImmunologyCancer researchbiology.proteinlcsh:QColitis UlcerativeDigestive SystemPloS one
researchProduct