Search results for "Respiratory Mucosa"

showing 10 items of 49 documents

Upregulation of activin-B and follistatin in pulmonary fibrosis: a translational study using human biopsies and a specific inhibitor in mouse fibrosi…

2014

Background: Activins are members of the TGF-ß superfamily of growth factors. First, we identified by expression array screening that activin-B and follistatin are upregulated in human idiopathic pulmonary fibrosis (IPF). Next, we wanted to clarify their specific role in lung fibrosis formation. Methods: We used specific antibodies for activin-A and -B subunits and follistatin to measure and localize their levels in idiopathic pulmonary fibrosis and control lung biopsies. To inhibit activin signaling, we used soluble activin type IIB receptor fused to the Fc portion of human IgG1 (sActRIIB-Fc) in two different mouse models of pulmonary fibrosis. Results: Activin-B and follistatin mRNA levels…

MalePathologyFollistatinPulmonary FibrosisPROTEINCell CountQuadriceps MuscleACTIVATIONIdiopathic pulmonary fibrosisMiceBMP-7FibrosisPulmonary fibrosisfollistatinInhibin-beta SubunitsGREMLINImmunity Cellularmedicine.diagnostic_testbiologyactivinsPIRFENIDONEPirfenidonerespiratory systemidiopathic pulmonary fibrosisMouse fibrosis model3. Good healthUp-RegulationActivinsmedicine.anatomical_structureACUTE EXACERBATIONmouse fibrosis modelembryonic structuresGROWTHBronchoalveolar Lavage Fluidhormones hormone substitutes and hormone antagonistsmedicine.drugResearch ArticleSignal TransductionPulmonary and Respiratory MedicineEXPRESSIONmedicine.medical_specialtyendocrine systemRecombinant Fusion ProteinseducationIdiopathic pulmonary fibrosisRespiratory MucosaAlveolar cellsINFLAMMATIONmedicineAnimalsHumansRNA MessengerLungbusiness.industrymedicine.diseaserespiratory tract diseasesMice Inbred C57BLPulmonary AlveoliDisease Models AnimalBronchoalveolar lavageProtein Biosynthesis3121 General medicine internal medicine and other clinical medicinebiology.proteinbusinessFollistatin
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Differential distribution of inflammatory cells in large and small airways in smokers

2007

BACKGROUND: Smoking induces structural changes in the airways, and is considered a major factor in the development of airflow obstruction in chronic obstructive pulmonary disease. However, differences in inflammatory cell distribution between large airways (LA) and small airways (SA) have not been systematically explored in smokers. Hypothesis: The content of cells infiltrating the airway wall differs between LA and SA. AIMS: To compare the content of neutrophils, macrophages, lymphocytes and mast cells infiltrating LA and SA in smokers who underwent surgery for lung cancer. METHODS: Lung tissue from 15 smokers was analysed. Inflammatory cells in the lamina propria were identified by immuno…

MalePathologymedicine.medical_specialtyLung NeoplasmsNeutrophilsCOPD inflammationCell CountInflammationRespiratory MucosaSettore MED/10 - Malattie Dell'Apparato RespiratorioLung injuryPathology and Forensic MedicineSmokeHumansMedicineLymphocytesMast CellsRespiratory systemLung cancerLungPhagocytesLamina propriaLungbusiness.industryMacrophagesSmokingGeneral MedicineMiddle Agedrespiratory systemmedicine.diseaseImmunohistochemistryrespiratory tract diseasesmedicine.anatomical_structureImmunologyImmunohistochemistryOriginal ArticleFemalemedicine.symptombusinessRespiratory tractJournal of Clinical Pathology
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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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Phosphodiesterase 4 inhibition decreases MUC5AC expression induced by epidermal growth factor in human airway epithelial cells

2005

Background: A common pathological feature of chronic inflammatory airway diseases such as asthma and chronic obstructive pulmonary disease (COPD) is mucus hypersecretion. MUC5AC is the predominant mucin gene expressed in healthy airways and is increased in asthmatic and COPD patients. Recent clinical trials indicate that phosphodiesterase type 4 (PDE4) inhibitors may have therapeutic value for COPD and asthma. However, their direct effects on mucin expression have been scarcely investigated. Methods: MUC5AC mRNA and protein expression were examined in cultured human airway epithelial cells (A549) and in human isolated bronchial tissue stimulated with epidermal growth factor (EGF; 25 ng/ml).…

MalePulmonary and Respiratory Medicinemedicine.medical_specialtyBlotting WesternBronchiEnzyme-Linked Immunosorbent AssayRespiratory MucosaMucin 5ACp38 Mitogen-Activated Protein KinasesWestern blotEpidermal growth factorInternal medicineGene expressionCyclic AMPmedicineHumansRNA MessengerPhosphotyrosineCells CulturedRoflumilastRolipramAgedA549 cellEpidermal Growth Factormedicine.diagnostic_testReverse Transcriptase Polymerase Chain Reactionbusiness.industryCilomilastMucinMucinsEpithelial CellsMiddle Agedrespiratory systemMolecular biologyRecombinant ProteinsCyclic Nucleotide Phosphodiesterases Type 4respiratory tract diseasesEndocrinology3'5'-Cyclic-AMP PhosphodiesterasesAirway BiologyFemalebusinessmedicine.drugThorax
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Nerve ablation after bronchial thermoplasty and sustained improvement in severe asthma

2017

Abstract Background Bronchial thermoplasty (BT) is a non-pharmacological intervention for severe asthma whose mechanism of action is not completely explained by a reduction of airway smooth muscle (ASM). In this study we analyzed the effect of BT on nerve fibers and inflammatory components in the bronchial mucosa at 1 year. Methods Endobronchial biopsies were obtained from 12 subjects (mean age 47 ± 11.3 years, 50% male) with severe asthma. Biopsies were performed at baseline (T0) and after 1 (T1), 2 (T2) and 12 (T12) months post-BT, and studied with immunocytochemistry and microscopy methods. Clinical data including Asthma Quality of Life Questionnaire (AQLQ) and Asthma Control Questionnai…

MaleSevere asthmaBronchial biopsieBiopsymedicine.medical_treatmentVital CapacityGastroenterologyBronchial thermoplasty0302 clinical medicineBronchoscopyQuality of lifeForced Expiratory VolumeSubmucosa030212 general & internal medicinemedicine.diagnostic_testCD68Middle AgedNerve fiberAblationImmunohistochemistryResidual VolumeTreatment Outcomemedicine.anatomical_structureAsthma Control QuestionnaireFemaleResearch ArticleAdultPulmonary and Respiratory Medicinemedicine.medical_specialtyBronchiBronchial biopsiesNerve fibersRespiratory MucosaSettore MED/10 - Malattie Dell'Apparato Respiratorio03 medical and health sciencesInternal medicineBronchoscopymedicineHumansAgedAsthmalcsh:RC705-779Bronchial thermoplastybusiness.industryTotal Lung Capacitylcsh:Diseases of the respiratory systemmedicine.diseaseAsthmarespiratory tract diseases030228 respiratory systembusinessBMC Pulmonary Medicine
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Increased airway inflammatory cells in endurance athletes: what do they mean?

2003

Inflammatory cells are increased in the airways of endurance athletes, but their role in causing exercise-induced respiratory symptoms and bronchoconstriction, or their possible long-term consequences, are uncertain.To put the results of athlete studies in perspective, by analysing the pathogenesis of airway cell changes and their impact on respiratory function.Athletes of different endurance sports at rest showed increased airway neutrophils. Elite swimmers and skiers also showed large increases in airway eosinophils and lymphocytes, possibly related to chronic, exercise-related exposure to irritants or cold and dry air, respectively. Post-exercise studies reported variable responses of ai…

NeutrophilsNeutrophilOsmolar ConcentrationRespiratory MucosaEosinophilLeukocyteSettore MED/10 - Malattie Dell'Apparato RespiratorioNitric OxideEosinophilsAsthma Exercise-InducedLeukocyte CountCell Adhesion MoleculeLeukocytesPhysical EnduranceHumansLymphocyteLymphocytesBronchial HyperreactivityCell Adhesion MoleculesHumanSports
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Phospho-p38 MAPK expression in COPD patients and asthmatics and in challenged bronchial epithelium

2015

<b><i>Background:</i></b> The role of mitogen-activated protein kinases (MAPK) in regulating the inflammatory response in the airways of patients with chronic obstructive pulmonary disease (COPD) and asthmatic patients is unclear. <b><i>Objectives:</i></b> To investigate the expression of activated MAPK in lungs of COPD patients and in bronchial biopsies of asthmatic patients and to study MAPK expression in bronchial epithelial cells in response to oxidative and inflammatory stimuli. <b><i>Methods:</i></b> Immunohistochemical expression of phospho (p)-p38 MAPK, p-JNK1 and p-ERK1/2 was measured in bronchial mucosa in pat…

P38 MAPKMaleMAPK/ERK pathwayAsthma phenotypeSMOKERespiratory SystemMitogen-activated protein kinases; p65; Pathology of chronic obstructive pulmonary disease; Chronic obstructive pulmonary disease phenotypes; Asthma phenotypesPathology of chronic obstructive pulmonary diseasep38 Mitogen-Activated Protein KinasesChronic obstructive pulmonary disease phenotypePulmonary Disease Chronic ObstructiveOXIDATIVE STRESSMACROPHAGESRespiratory systemMitogen-activated protein kinasesChronic obstructive pulmonary disease phenotypesMitogen-activated protein kinases; p65; pathology of chronic obstructive pulmonary disease phenotypes; asthma phenotypesCOPDp65KinaseAsthma phenotypes; Chronic obstructive pulmonary disease phenotypes; Mitogen-activated protein kinases; p65; Pathology of chronic obstructive pulmonary disease; Pulmonary and Respiratory MedicineACTIVATED PROTEIN-KINASEInterleukinMiddle AgedImmunohistochemistrypathology of chronic obstructive pulmonary disease phenotypesAsthma phenotypesFemaleLife Sciences & BiomedicinePulmonary and Respiratory Medicinep38 mitogen-activated protein kinasesBlotting WesternINHIBITIONSocio-culturaleBronchiRespiratory MucosaOBSTRUCTIVE PULMONARY-DISEASE1102 Cardiovascular Medicine And HaematologyCell LinemedicineHumansLymphocyte CountInterleukin 8AgedAsthmaScience & Technologybusiness.industryInterleukin-8Transcription Factor RelAPATHWAYSMitogen-activated protein kinasemedicine.diseaseAsthmarespiratory tract diseasesSEVERITYCase-Control StudiesCELLSImmunologybusiness
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Subcellular distribution of choline acetyltransferase by immunogold electron microscopy in non-neuronal cells: Placenta, airways and murine embryonic…

2012

Abstract Aims Acetylcholine is synthesized in more or less all mammalian cells. However, little is known about the subcellular location of acetylcholine synthesis. Therefore, in the present experiments the subcellular location of the synthesizing enzyme choline acetyltransferase (ChAT) was investigated by anti-ChAT immunogold electron microscopy in human placenta and airways as well as in a murine embryonic stem cell line (CGR8 cell line). Main methods Human tissue was obtained as so-called surplus tissue (after delivery/surgical removal because of lung tumor); the CGR8 stem cell line was cultured under standard conditions. For human tissue a monoclonal mouse anti-ChAT antibody (ab) was use…

PlacentaeducationBronchiRespiratory MucosaBiologyGeneral Biochemistry Genetics and Molecular BiologyCell LineCholine O-AcetyltransferaseCell membraneMicePregnancyCaveolaeMacrophages Alveolarmental disordersmedicineAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsNuclear membraneCells CulturedEmbryonic Stem Cellshealth care economics and organizationsEpithelial CellsGeneral MedicineImmunogold labellingImmunohistochemistryCholine acetyltransferaseMolecular biologyCellular StructureshumanitiesTrophoblastsCell biologyMicroscopy ElectronCytosolCell nucleusmedicine.anatomical_structureCell cultureFemaleLife Sciences
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Cationic polyaspartamide-based nanocomplexes mediate siRNA entry and down-regulation of the pro-inflammatory mediator high mobility group box 1 in ai…

2015

Abstract High-mobility group box 1 (HMGB1) is a nonhistone protein secreted by airway epithelial cells in hyperinflammatory diseases such as asthma. In order to down-regulate HMGB1 expression in airway epithelial cells, siRNA directed against HMGB1 was delivered through nanocomplexes based on a cationic copolymer of poly(N-2-hydroxyethyl)- d,l -aspartamide (PHEA) by using H441 cells. Two copolymers were used in these experiments bearing respectively spermine side chains (PHEA-Spm) and both spermine and PEG2000 chains (PHEA-PEG-Spm). PHEA-Spm and PHEA-PEG-Spm derivatives complexed dsDNA oligonucleotides with a w/w ratio of 1 and higher as shown by a gel retardation assay. PHEA-Spm and PHEA-P…

Polyaspartamide copolymerNucleic acid-based drugDown-RegulationPharmaceutical ScienceSpermineRespiratory MucosaBiologyTransfectionAirway epithelial cellsNucleic acid-based drugsFlow cytometrychemistry.chemical_compoundCell Line TumorMaterials TestingAirway epithelial cellmedicineHumansElectrophoretic mobility shift assayMTT assayDAPIRNA Small InterferingCytotoxicityPolyhydroxyethyl MethacrylateHMGB1Airway epithelial cells; HMGB1; Nucleic acid-based drugs; PHEA; Polyaspartamide copolymers; Sirnamedicine.diagnostic_testOligonucleotideMammaglobin AfungiGene Transfer TechniquesEpithelial CellsDNAPHEAMolecular biologyNanostructuresPolyaspartamide copolymerschemistrySirnaTrypan bluePeptides
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PEGYLATED POLYASPARTAMIDE–POLYLACTIDE BASED NANOPARTICLES PENETRATING CYSTIC FIBROSIS ARTIFICIAL MUCUS

2016

Here, the preparation of mucus-penetrating nanoparticles for pulmonary administration of ibuprofen in patients with cystic fibrosis is described. A fluorescent derivative of α,β-poly(N-2-hydroxyethyl)-D,L-aspartamide is synthesized by derivatization with rhodamine, polylactide, and poly(ethylene glycol), to obtain polyaspartamide− polylactide derivatives with different degrees of pegylation. Starting from these copolymers, fluorescent nanoparticles with different poly(ethylene glycol) content, empty and loaded with ibuprofen, showed spherical shape, colloidal size, slightly negative ζ potential, and biocompatibility toward human bronchial epithelial cells. The high surface poly(ethylene gly…

Polymers and PlasticsBiocompatibilityPolyestersαL-aspartamideNanoparticleBioengineeringIbuprofen02 engineering and technologyRespiratory Mucosa010402 general chemistry01 natural sciencesCell LinePolyethylene GlycolsBiomaterialsRhodaminecystic fibrosischemistry.chemical_compoundpolymeric nanoparticles cystic fibrosis αβ-poly(N-2-hydroxyethyl)-DL-aspartamideMaterials ChemistryCopolymerOrganic chemistryHumansDerivatizationβ-poly(N-2-hydroxyethyl)-Dpolymeric nanoparticles; cystic fibrosis; α; β-poly(N-2-hydroxyethyl)-D; L-aspartamide021001 nanoscience & nanotechnologyMucus0104 chemical sciencesMucuspolymeric nanoparticleschemistrySettore CHIM/09 - Farmaceutico Tecnologico ApplicativoPEGylationNanoparticles0210 nano-technologyPeptidesEthylene glycolNuclear chemistry
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