Search results for "macrophages"

showing 10 items of 533 documents

In vitro study of human alveolar macrophage and peripheral blood mononuclear cell reactive oxygen-intermediates release induced by sulfur dioxide at …

1994

Sulfur dioxide (SO2) is a major air pollutant in urban areas. Alveolar macrophages (AM) located on the alveolar surface are in direct contact with this inhaled gas. We evaluated the dose-dependent effect of SO2 exposure on the oxidative metabolism of AM and peripheral blood mononuclear cells (PBMNC) by measuring the spontaneous and stimulated reactive oxygen intermediates (ROI) release. AM or PBMNC were placed on a polycarbonate membrane, which was in direct contact with the surface of a nutrient reservoir. For exposure of the cells to SO2 a special chamber was employed, in which humidified standard air with 5% CO2 at 37 degrees C was mixed with SO2 at the desired concentration. Periods of …

MalePulmonary and Respiratory MedicineTime Factorschemistry.chemical_elementStimulationIn Vitro Techniquescomplex mixturesOxygenPeripheral blood mononuclear cellchemistry.chemical_compoundMacrophages AlveolarHumansSulfur DioxideIn vitro studyCells CulturedSulfur dioxidePollutantChromatographyDose-Response Relationship DrugChemistryMiddle Agedrespiratory tract diseasesLuminescent MeasurementsImmunologyLeukocytes MononuclearAlveolar macrophageFemaleReactive Oxygen SpeciesBronchoalveolar Lavage FluidPolycarbonate membraneLung
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Patterns of Inflammatory Responses in Large and Small Airways in Smokers with and without Chronic Obstructive Pulmonary Disease

2010

<i>Background:</i> Chronic obstructive pulmonary disease (COPD) is characterised by progressive and irreversible airway obstruction. Smoking causes persistent inflammation in lung tissue. However, differences in inflammatory responses between the large and small airways have not been systematically explored among smokers with and without COPD. <i>Objectives:</i> The aim of our research was to characterise the expression and localisation of NF-ĸBp65 and histone deacetylase 2 (HDAC2) as well as inflammatory cell (macrophages, lymphocytes, neutrophils) distribution in large and small airways, in nonsmokers and in smokers with and without COPD. <i>Methods:</i&gt…

MalePulmonary and Respiratory Medicinemedicine.medical_specialtyNeutrophilsHistone Deacetylase 2Pulmonary diseaseBronchiCell CountInflammationCD8-Positive T-Lymphocytesurologic and male genital diseasesPersistent inflammationPulmonary Disease Chronic ObstructiveRisk FactorsCarcinoma Non-Small-Cell LungInternal medicineMacrophages AlveolarCarcinomamedicineHumansLungAgedCOPDSmall airwaysbusiness.industrySmokingRespiratory diseaseTranscription Factor RelAMiddle Agedrespiratory systemAirway obstructionmedicine.diseaseImmunohistochemistryrespiratory tract diseasesImmunologyDisease ProgressionCardiologyFemalemedicine.symptombusinessRespiration
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Evidence that C1q, a Subcomponent of the First Component of Complement, is an Fc Receptor of Peritoneal and Alveolar Macrophages

1980

Abstract Guinea pig peritoneal macrophages were cultured for 24 h in the presence of two inhibitors of the biosynthesis of collagen-like molecules such as C1q : 10 -3 M 3,4-dehydroproline or 10 -4 M 2,2′-dipyridyl. Their Fc-receptor activity was measured by rosette formation, using sheep erythrocytes (E) coated with rabbit anti-sheep IgG (EA IgG ). The Fc-receptor activity was decreased by 40 to 70% of control cultures depending on the amount of IgG on the E. The activity of a second receptor on the macrophages, mediating the binding of C3b coated E, was not altered by this treatment. Rat alveolar macrophages were depleted of their Fc-receptor activity by pronase treatment (1.5 mg/ml) in th…

MaleRosette FormationProlineGuinea PigsImmunologyFc receptorReceptors FcPronaseGuinea pigchemistry.chemical_compound22'-DipyridylBiosynthesisComplement C1AnimalsAscitic FluidImmunology and AllergySecretionReceptorIncubationbiologyMacrophagesComplement C3HematologyMolecular biologyRatsReceptors ComplementPulmonary AlveoliMembraneBiochemistrychemistryPronasebiology.proteinFemaleImmunobiology
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Extracellular Nampt promotes macrophage survival via a nonenzymatic interleukin-6/STAT3 signaling mechanism.

2008

Macrophages play key roles in obesity-associated pathophysiology, including inflammation, atherosclerosis, and cancer, and processes that affect the survival-death balance of macrophages may have an important impact on obesity-related diseases. Adipocytes and other cells secrete a protein called extracellular nicotinamide phosphoribosyltransferase (eNampt; also known as pre-B cell colony enhancing factor or visfatin), and plasma levels of eNampt increase in obesity. Herein we tested the hypothesis that eNampt could promote cell survival in macrophages subjected to endoplasmic reticulum (ER) stress, a process associated with obesity and obesity-associated diseases. We show that eNampt potent…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCell SurvivalNicotinamide phosphoribosyltransferaseApoptosisBiologyEndoplasmic ReticulumBiochemistryStat3 Signaling Pathwaychemistry.chemical_compoundParacrine signallingMicePiperidinesInternal medicinemedicineAnimalsSecretionAutocrine signallingSTAT3Nicotinamide PhosphoribosyltransferaseMolecular BiologyNicotinamide MononucleotideNicotinamide mononucleotideAcrylamidesInterleukin-6MacrophagesMechanisms of Signal TransductionCell BiologyCell biologyMice Inbred C57BLEndocrinologychemistryGene Expression Regulationbiology.proteinCytokinesSignal transductionSignal TransductionThe Journal of biological chemistry
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Interruption of Macrophage-Derived IL-27(p28) Production by IL-10 during Sepsis Requires STAT3 but Not SOCS3

2014

Abstract Severe sepsis and septic shock are leading causes of morbidity and mortality worldwide. Infection-associated inflammation promotes the development and progression of adverse outcomes in sepsis. The effects of heterodimeric IL-27 (p28/EBI3) have been implicated in the natural course of sepsis, whereas the molecular mechanisms underlying the regulation of gene expression and release of IL-27 in sepsis are poorly understood. We studied the events regulating the p28 subunit of IL-27 in endotoxic shock and polymicrobial sepsis following cecal ligation and puncture. Neutralizing Abs to IL-27(p28) improved survival rates, restricted cytokine release, and reduced bacterial burden in C57BL/…

MaleSTAT3 Transcription Factormedicine.medical_treatmentImmunologySuppressor of Cytokine Signaling ProteinsInflammationSpleenBiologyArticleSepsisMiceSepsismedicineAnimalsHumansImmunology and AllergyReceptors CytokineAntibodies BlockingCecumCells CulturedMice KnockoutSeptic shockInterleukinsMacrophagesReceptors Interleukinmedicine.diseaseBacterial LoadInterleukin-10Mice Inbred C57BLToll-Like Receptor 4Adaptor Proteins Vesicular TransportDisease Models AnimalOxidative StressInterleukin 10Cytokinemedicine.anatomical_structureIntegrin alpha MSuppressor of Cytokine Signaling 3 ProteinMyeloid Differentiation Factor 88ImmunologyTLR4biology.proteinmedicine.symptomJournal of Immunology
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Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.

2011

BackgroundIt is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of Hsp60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro analyses.Methods and resultsBronchial biopsies from patients with stable COPD, smoker controls with normal lung function, and non-smoker controls were studied. We quantified by immunohistochemistry levels of Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and HSF-1, along with levels of inflammatory markers. Hsp10, Hsp40, and Hsp60 were increased during progression of disease. We found also a positive correlation between th…

MaleSTRESSPulmonologyChronic Obstructive Pulmonary DiseasesNeutrophilsBiopsyGene ExpressionCD8-Positive T-Lymphocytesmedicine.disease_causeBiochemistryEpitheliumPulmonary function testingPathogenesisACTIVATIONPulmonary Disease Chronic ObstructiveMolecular Cell BiologyLungCOPDMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionCOPD Hsp60QRCOPD heat shock proteins inflammationMiddle AgedImmunohistochemistrymedicine.anatomical_structureEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISMedicineFemalemedicine.symptomInflammation MediatorsSPINAL-CORDResearch ArticleEXPRESSIONanimal structuresCOPD; heat shock proteins; inflammationScienceImmunologyMolecular Sequence DataInflammationBronchichemical and pharmacologic phenomenaHEAT-SHOCK-PROTEIN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS ACUTE LUNG INJURY SPINAL-CORD CELL-DEATH KAPPA-B HEAT-SHOCK-PROTEIN-60 STRESS EXPRESSION ACTIVATIONKAPPA-BBiologyHEAT-SHOCK-PROTEINMicrobiologycomplex mixturesCell LineACUTE LUNG INJURYMolecular GeneticsIn vivoStress PhysiologicalHeat shock proteinmedicineGeneticsHumansCOPDRNA MessengerBiologyAgedLungMucous MembraneBase SequenceSettore BIO/16 - Anatomia UmanaMacrophagesfungiImmunityTranscription Factor RelAProteinsComputational BiologyChaperonin 60medicine.diseaseChaperone Proteinsrespiratory tract diseasesGene Expression RegulationCELL-DEATHHEAT-SHOCK-PROTEIN-60inflammationImmunologyheat shock proteinsClinical ImmunologyOxidative stressBiomarkers
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Interleukin (IL)-22 receptor 1 is over-expressed in primary Sjogren's syndrome and Sjögren-associated non-Hodgkin lymphomas and is regulated by IL-18.

2015

Summary The aim of this study was to elucidate more clearly the role of interleukin (IL)-18 in modulating the IL-22 pathway in primary Sjögren's syndrome (pSS) patients and in pSS-associated lymphomas. Minor salivary glands (MSGs) from patients with pSS and non-specific chronic sialoadenitis (nSCS), parotid glands biopsies from non-Hodgkin lymphomas (NHL) developed in pSS patients, were evaluated for IL-18, IL-22, IL-22 receptor 1 (IL-22R1), IL-22 binding protein (IL-22BP) and signal transducer and activator of transcription-3 (STAT-3) expression. MSGs IL-22R1-expressing cells were characterized by confocal microscopy and flow cytometry in pSS, nSCS and healthy controls. The effect of recom…

MaleSalivary Glandslaw.inventionInterleukin 22lawIL-22Immunology and AllergyMyeloid CellsIL-22R1Receptormedicine.diagnostic_testnon-Hodgkin lymphomaLymphoma Non-HodgkinInterleukin-17TranslationalInterleukin-18Lacrimal ApparatusInterleukinMiddle AgedHaematopoiesisSjogren's SyndromeIL-22BPRecombinant DNASjögren's syndromeInterleukin 18FemaleIL-18Signal TransductionAdultSTAT3 Transcription FactorImmunologyPrimary Cell CultureBiologyPeripheral blood mononuclear cellIL-18; IL-22; IL-22BP; IL-22R1; Sjögren's syndrome; non-Hodgkin lymphomaSialadenitisFlow cytometrystomatognathic systemmedicineHumansAgedInterleukinsMacrophagesReceptors InterleukinSettore MED/16 - Reumatologiastomatognathic diseasesGene Expression RegulationImmunologyLeukocytes MononuclearClinical and experimental immunology
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Immunoproteasome LMP2 60HH Variant Alters MBP Epitope Generation and Reduces the Risk to Develop Multiple Sclerosis in Italian Female Population

2010

BackgroundAlbeit several studies pointed out the pivotal role that CD4+T cells have in Multiple Sclerosis, the CD8+ T cells involvement in the pathology is still in its early phases of investigation. Proteasome degradation is the key step in the production of MHC class I-restricted epitopes and therefore its activity could be an important element in the activation and regulation of autoreactive CD8+ T cells in Multiple Sclerosis.Methodology/principal findingsImmunoproteasomes and PA28-alphabeta regulator are present in MS affected brain area and accumulated in plaques. They are expressed in cell types supposed to be involved in MS development such as neurons, endothelial cells, oligodendroc…

MaleT cells proteasomes multiple sclerosis parietal lobeMuscle ProteinsImmunoproteasomeEpitopeEpitopesGene FrequencyRisk FactorsCytotoxic T cellFunding: This work was financed in part by the grant Giovani Ricercatori 2007 from Italian Ministry of Health to MM DG and FMB by a grant from the European Commission Integrated Project PROTEOMAGE (FP6) to CF by the finalized projects of Fondazione Italiana Sclerosi Multipla (FISM) cod. 2003/R26 and BioPharmaNet to CF and 2002/R/40 and 2005/R/10 2008/R/11 (Genoa) to SD'A by the University of Bologna (FRO) to MPF by the Regione Piemonte (Ricerca Sanitaria Finalizzata Project and Ricerca Sanitaria Applicata-CIPE Project) to SD'A by Associazione Amici del Centro Dino Ferrari and IRCCS Ospedale Maggiore Policlinico Milano to DG and by the grants Sonderforschungsbereich (SFB-507 SFB-421) to PMK and US the grants TR43 and Neurocure to PMK. MM benefited from the A.V. Humboldt PostDoc fellowship. The funders had no role in study design data collection and analysis decision to publish or preparation of the manuscript.MultidisciplinaryMicrogliaQRBrainMiddle AgedImmunohistochemistryCysteine EndopeptidasesOligodendrogliamedicine.anatomical_structureItalyImmunoproteasome; multiple sclerosis; italian populationmultiple sclerosiImmunology/Antigen Processing and RecognitionMedicineFemaleMicrogliaNeuroscience/Neurobiology of Disease and RegenerationResearch ArticleProtein BindingAdultProteasome Endopeptidase ComplexMultiple SclerosisGenotypeScienceMolecular Sequence DataImmunology/AutoimmunityBiologySex FactorsMHC class IHLA-A2 AntigenmedicineHumansAmino Acid SequenceAlleleHLA-A AntigensMultiple sclerosisMacrophagesMyelin Basic Proteinmedicine.diseaseMyelin basic proteinImmunologybiology.proteinitalian populationCD8PLoS ONE
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Effects of titanium dioxide pigments on mouse peritoneal macrophages in vivo.

1982

MaleTitaniumHealth Toxicology and MutagenesisMacrophagesAcid PhosphataseCell CountGeneral MedicinePigments BiologicalToxicologyPollutionPigmentchemistry.chemical_compoundMicechemistryPhagocytosisIn vivovisual_artEnvironmental chemistryTitanium dioxidevisual_art.visual_art_mediumEcotoxicologyAnimalsAscitic FluidGlucuronidaseBulletin of environmental contamination and toxicology
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Vitamin D Receptor Activation Reduces Angiotensin-II–Induced Dissecting Abdominal Aortic Aneurysm in Apolipoprotein E–Knockout Mice

2015

Objective— Abdominal aortic aneurysm (AAA) is a vascular disorder characterized by chronic inflammation of the aortic wall. Low concentrations of vitamin D 3 are associated with AAA development; however, the potential direct effect of vitamin D 3 on AAA remains unknown. This study evaluates the effect of oral treatment with the vitamin D 3 receptor (VDR) ligand, calcitriol, on dissecting AAA induced by angiotensin-II (Ang-II) infusion in apoE −/− mice. Approach and Results— Oral treatment with calcitriol reduced Ang-II–induced dissecting AAA formation in apoE −/− mice, which was unrelated to systolic blood pressure or plasma cholesterol concentrations. Immunohistochemistry and reverse-tran…

MaleVascular Endothelial Growth Factor A0301 basic medicineDissecting Abdominal Aortic Aneurysm030204 cardiovascular system & hematologyLigandsCalcitriol receptorchemistry.chemical_compound0302 clinical medicineAorta AbdominalCells CulturedMice KnockoutAngiotensin IIVascular endothelial growth factorChemotaxis LeukocyteVascular endothelial growth factor APhenotypeMatrix Metalloproteinase 9Vitamin D3 ReceptorMatrix Metalloproteinase 2RNA Interferencelipids (amino acids peptides and proteins)ChemokinesMitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineSignal Transductionmedicine.drugmedicine.medical_specialtyCalcitriolBiologyTransfectionProinflammatory cytokine03 medical and health sciencesApolipoproteins ECalcitriolInternal medicineHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansGenetic Predisposition to DiseaseRetinoid X Receptor alphaMacrophagesAngiotensin IIMice Inbred C57BLAortic DissectionDisease Models Animal030104 developmental biologyEndocrinologychemistryReceptors CalcitriolAortic Aneurysm AbdominalArteriosclerosis, Thrombosis, and Vascular Biology
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