Search results for "NEUTROPHIL"

showing 10 items of 449 documents

Proteome analysis of myocardial tissue following ischemia and reperfusion--effects of complement inhibition.

2006

Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic mediators, release of cytokines, leukocyte accumulation, and subsequent severe tissue injury. In this regard, activation of transcription factors (i.e., NFkappaB) and de novo protein synthesis or inflammatory protein degradation seems to play an important role. In the present study, we analyzed the cardiac protein expression following myocardial ischemia (60 min) and reperfusion (180 min) in a rabbit model utilizing two-dimensional electrophoresis and nanoHPLC/ESI-MS/MS for biochemical protein identification. To achieve cardioprotective effects, we used a novel highly selective smal…

MaleProteomeG proteinNeutrophilsMolecular Sequence DataBiophysicsIschemiaMyocardial IschemiaMyocardial Reperfusion InjuryProtein degradationComplement C1 Inactivator ProteinsBiochemistryAnalytical ChemistrySuperoxide dismutaseClassical complement pathwayElectrocardiographyNecrosismedicineProtein biosynthesisAnimalsAmino Acid SequenceMolecular BiologyCreatine KinasebiologySuperoxide DismutaseMyocardiumalpha-Crystallin B ChainComplement System Proteinsmedicine.diseaseMolecular biologyComplement systembiology.proteinCreatine kinaseRabbitsMicrotubule-Associated ProteinsBiomarkersBiochimica et biophysica acta
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Association of increased CCL5 and CXCL7 chemokine expression with neutrophil activation in severe stable COPD

2009

BACKGROUND: Increased numbers of activated neutrophils have been reported in the bronchial mucosa of patients with stable chronic obstructive pulmonary disease (COPD), particularly in severe disease. OBJECTIVES: To investigate the expression of neutrophilic chemokines and adhesion molecules in bronchial biopsies from patients with stable COPD of different severity (GOLD stages I-IV) compared with age-matched control subjects, smokers with normal lung function and never smokers. METHODS: The expression of CCL5, CXCL1, 5, 6, 7 and 8, CXCR1, CXCR2, CD11b and CD44 was measured in the bronchial mucosa using immunohistochemistry, confocal immunofluorescence, real-time quantitative polymerase chai…

MalePulmonary and Respiratory MedicineChemokinePathologymedicine.medical_specialtyCOPD neutrophils bronchial mucosa CCL5 CXCL7BronchiRespiratory MucosaGranulocyteNeutrophil ActivationCCL5Pulmonary Disease Chronic ObstructiveneutrophilsSubmucosaCOPDHumansMedicineCXC chemokine receptorsChemokine CCL5AgedCOPDbronchial mucosaCCL5biologySettore BIO/16 - Anatomia UmanaCD11 Antigensbusiness.industryCD44Epithelial CellsMiddle Agedrespiratory systemmedicine.diseaseRespiratory Function Testsrespiratory tract diseasesCXCL1Hyaluronan Receptorsmedicine.anatomical_structureAcute DiseaseImmunologyCXCL7biology.proteinFemaleLeukocyte ElastasebusinessCOPD; neutrophils; bronchial mucosa; CCL5; CXCL7Chemokines CXCCOPD CCL5CXCL7NEUTROPHILThorax
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Airway inflammation in patients affected by obstructive sleep apnea syndrome

2004

Obstructive sleep apnea syndrome (OSAS) has been shown to be associated to upper airway inflammation. The object of the present study was to establish the presence of bronchial inflammation in OSAS subjects. In 16 subjects affected by OSAS, and in 14 healthy volunteers, airway inflammation was detected by the cellular analysis of the induced sputum. OSAS patients, as compared to control subjects, showed a higher percentage of neutrophils (66.7+/-18.9 vs. 25.8+/-15.6) (P<0.001) and a lower percentage of macrophages (29.4+/-18.4 vs. 70.8+/-15.3) (P<0.001). The percentage of eosinophils and lymphocytes were not significantly different in the two groups. OSAS subjects show bronchial inflammatio…

MalePulmonary and Respiratory MedicineNeutorphilSputum Cytologymedicine.medical_specialtyPathologyNeutrophilsInflammationGranulocyteGastroenterologyBody Mass IndexLeukocyte CountInternal medicinemedicineHumansInduced sputumBronchitisAgedSleep Apnea Obstructivebusiness.industryMacrophagesSputumSleep apneaOSASMiddle Agedmedicine.diseaserespiratory tract diseasesObstructive sleep apneamedicine.anatomical_structureNeutrophil InfiltrationOSAS; Neutrophils; Induced sputumBronchitisSputumFemalemedicine.symptombusinessBody mass index
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Similarity and differences in elderly patients with fixed airflow obstruction by asthma and by chronic obstructive pulmonary disease

2008

SummaryBackgroundEpidemiologic studies have demonstrated that elderly patients with fixed airflow obstruction can be affected by asthma or chronic obstructive pulmonary disease (COPD).MethodsWe studied 49 consecutive elderly outpatients, presenting fixed airflow obstruction, by clinical history (smoking), pulmonary function tests, blood gas analysis, and induced sputum.ResultsThe age was not different in patients with COPD (n=28) and asthma (n=21) (70.2±3.9 years vs. 69.6±3.7 years), also the degree of fixed airflow obstruction was similar (FEV1: 58.3±1.5% vs. 59.0±1.4% of predicted). Patients with asthma had significantly more eosinophils in peripheral blood (0.43±0.05×10−3μL vs. 0.27±0.1×…

MalePulmonary and Respiratory MedicineVital capacitymedicine.medical_specialtySettore MED/09 - Medicina Internaasthma chronic obstructive pulmonary disease.NeutrophilsVital Capacitychronic obstructive pulmonary disease.GastroenterologyPulmonary function testingPulmonary Disease Chronic ObstructiveFEV1/FVC ratioElderlyDLCOForced Expiratory VolumeInternal medicinemedicineHumanselderly patients; fixed airflow obstruction; asthma; chronic obstructive pulmonary disease.AgedAsthmaCOPDEosinophil cationic proteinbusiness.industryChronic obstructive pulmonary diseasefixed airflow obstructionRespiratory diseaseSputumasthmamedicine.diseaseRespiratory Function Testselderly patientrespiratory tract diseasesSurgeryEosinophilsFemalebusinessRespiratory Medicine
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Patterns of Inflammatory Responses in Large and Small Airways in Smokers with and without Chronic Obstructive Pulmonary Disease

2010

&lt;i&gt;Background:&lt;/i&gt; 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. &lt;i&gt;Objectives:&lt;/i&gt; 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. &lt;i&gt;Methods:&lt;/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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In vitro anti-inflammatory effects of AZD8999, a novel bifunctional muscarinic acetylcholine receptor antagonist /β2-adrenoceptor agonist (MABA) comp…

2019

Recent evidence indicates that AZD8999 (LAS190792), a novel muscarinic acetylcholine receptor antagonist and β2-adrenoceptor agonist (MABA) in development for chronic respiratory diseases, induces potent and sustained relaxant effects in human bronchi by adressing both muscarinic acetylcholine receptors and β2-adrenoceptor. However, the anti-inflammatory effects of the AZD8999 monotherapy or in combination with corticosteroids are unknown. This study investigates the anti-inflammatory effects of AZD8999 in monotherapy and combined with fluticasone propionate in neutrophils from healthy and chronic obstructive pulmonary disease (COPD) patients. Peripheral blood neutrophils from healthy and C…

MalePulmonologyNeutrophilsPhysiologyAnti-Inflammatory AgentsPharmacologyPathology and Laboratory MedicineBiochemistryPulmonary Disease Chronic ObstructiveWhite Blood CellsGlucocorticoid receptorAnimal CellsMuscarinic acetylcholine receptorMedicine and Health SciencesPost-Translational ModificationPhosphorylationReceptorImmune ResponseMultidisciplinaryPharmaceuticsQRDrug SynergismMiddle AgedReceptors MuscarinicHealthy VolunteersBody FluidsChemistryBloodPhysical SciencesQuinolinesMedicineDrug Therapy CombinationFemalemedicine.symptomCellular TypesAnatomymedicine.drugResearch ArticleSignal TransductionAgonistTransmembrane Receptorsmedicine.drug_classp38 mitogen-activated protein kinasesChronic Obstructive Pulmonary DiseaseImmune CellsScienceImmunologyInflammationMuscarinic AntagonistsThiophenesFluticasone propionateSigns and SymptomsDrug TherapyCyclohexanesDiagnostic MedicinemedicineHumansAdrenergic beta-2 Receptor AgonistsAgedInflammationBlood CellsDose-Response Relationship Drugbusiness.industryAntagonistChemical CompoundsBiology and Life SciencesProteinsCell BiologyAcetylcholine ReceptorsFluticasoneMuscarinic Acetylcholine ReceptorsReceptors Adrenergic beta-2PropionatesbusinessReceptor Antagonist TherapyPLoS ONE
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Co-option of Neutrophil Fates by Tissue Environments

2020

Classically considered short-lived and purely defensive leukocytes, neutrophils are unique in their fast and moldable response to stimulation. This plastic behavior may underlie variable and even antagonistic functions during inflammation or cancer, yet the full spectrum of neutrophil properties as they enter healthy tissues remains unexplored. Using a new model to track neutrophil fates, we found short but variable lifetimes across multiple tissues. Through analysis of the receptor, transcriptional, and chromatin accessibility landscapes, we identify varying neutrophil states and assign non-canonical functions, including vascular repair and hematopoietic homeostasis. Accordingly, depletion…

MaleReceptors CXCR4Transcription GeneticAngiogenesisNeutrophilsMedizinNeovascularization PhysiologicInflammationBiologyCXCR4General Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineSingle-cell analysismedicineNuclear Receptor Subfamily 4 Group A Member 1AnimalsCell LineageReceptorLung030304 developmental biology0303 health sciencesInnate immune systemChromatinChromatinCell biologyHematopoiesisIntestinesMice Inbred C57BLOrgan SpecificityFemalemedicine.symptomSingle-Cell AnalysisTranscriptome030217 neurology & neurosurgeryHomeostasisCell
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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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Two‐dimensional analysis of myocardial protein expression following myocardial ischemia and reperfusion in rabbits

2002

Myocardial ischemia and reperfusion injury (MI/R) can be related to leukocyte activation with subsequent release of cytokines and oxygen derived free radicals. Activation of the complement system has been implicated in the pathogenesis of myocardial ischemia and reperfusion injury. Inflammatory injury will subsequently result in cellular activation and protein synthesis. In the present study we analyzed the myocardial protein expression and its pattern following myocardial ischemia and reperfusion, with and without complement inhibition with the synthetic serine protease inhibitor Futhan/nafamstat mesilate (FUT-175) known to inhibit classical and alternative complement pathway in a rabbit m…

MaleSerine Proteinase InhibitorsNecrosisProteomeNeutrophilsMyocardial IschemiaIschemiaMyocardial Reperfusion InjuryPharmacologyGuanidinesBiochemistrySuperoxide dismutaseNecrosisRandom AllocationComplement inhibitormedicineAnimalsElectrophoresis Gel Two-DimensionalCreatine KinaseMolecular BiologybiologySuperoxide DismutaseChemistryGene Expression ProfilingMyocardiumHemodynamicsProteinsalpha-Crystallin B Chainmedicine.diseaseBenzamidinesComplement systemBiochemistrybiology.proteinAlternative complement pathwayCreatine kinaseRabbitsmedicine.symptomReperfusion injuryPROTEOMICS
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Inhibition of phospholipase A2 activities and some inflammatory responses by the marine product ircinin

1996

The marine product ircinin has been tested for its effects on secretory and cytosolic phospholipase A2 (PLA2) activities in vitro as well as for inhibition of cellular functions in human neutrophils and inflammatory responses in mice. Ircinin inhibited Naja naja venom, human synovial recombinant, bee venom and zymosan-injected rat air pouch PLA2 with IC50 values in the microM range, similar to those of the known inhibitor scalaradial. On the other hand, ircinin was less active on cytosolic PLA2 from human monocytes and decreased potently the release of LTB4 in human neutrophils. This marine product affected weakly human neutrophil functions like superoxide generation and degranulation. In t…

MaleSesterterpenesNeutrophilsAnti-Inflammatory AgentsInflammationPharmacologyPhospholipases AMicechemistry.chemical_compoundPhospholipase A2SuperoxidesIn vivomedicineAnimalsEdemaHumansPharmacologyAnalysis of VarianceDose-Response Relationship DrugbiologyTerpenesSuperoxideDegranulationGeneral MedicineLeukotriene A4In vitroPoriferaRatsPhospholipases A2CytosolchemistryBiochemistryMyeloperoxidasebiology.proteinHomosteroidsMarine Toxinslipids (amino acids peptides and proteins)medicine.symptomLeukocyte ElastaseNaunyn-Schmiedeberg's Archives of Pharmacology
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