Search results for "Smok"

showing 10 items of 769 documents

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
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Passive exposure to nicotine from e-cigarettes

2016

A procedure based on the use of ion mobility spectrometry (IMS), after liquid-liquid microextraction (LLME), has been successfully employed for the determination of passive exposure to nicotine from cigarette and e-cigarette smoking. Nicotine has been determined in exhaled breath and oral fluids of both, active and passive smokers. The aforementioned studies, made in closed environments, evidenced that the exhaled breath after conventional blend cigarette smoke provides nicotine levels of the order of 220 ng per puff, in the case of experienced smokers, being exhaled only 32 ng in the case of e-cigarettes. On the other hand, the nicotine amount in oral fluids of passive vapers was between 8…

Bodily SecretionsNicotineLiquid Phase MicroextractionElectronic Nicotine Delivery Systems01 natural sciencesAnalytical ChemistryNicotine03 medical and health sciences0302 clinical medicinemedicineHumansCigarette smoke030212 general & internal medicineChromatographyChemistry010401 analytical chemistryEnvironmental ExposurePassive ExposureEnvironmental exposureExhaled air0104 chemical sciencesBreath TestsOral fluidTobacco Smoke PollutionBodily secretionsmedicine.drugTalanta
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IL-17A induces chromatin remodeling promoting IL-8 release in bronchial epithelial cells: Effect of Tiotropium

2016

Abstract Aims IL-17A plays a key role in the persistence of airway inflammation, oxidative stress, and reduction of steroid-sensitivity in COPD. We studied the effect of IL-17A on chromatin remodeling and IL-8 production. Main methods We measured the levels of IL-8 and IL-17A in induced sputum supernatants (ISS) from healthy controls (HCs), healthy smokers (HSs), and COPD patients by enzyme-linked immunosorbent assay (ELISA). A human bronchial epithelial cell line (16HBE) was stimulated with ISS from HCs, HSs, or COPD subjects. IL-8 was evaluated in 16HBE by Western blot and real-time polymerase chain reaction (PCR). Histone deacetylase 2 (HDAC2), acetyl histone H3 (Ac-His H3) (k9) and inhi…

Bronchial epithelial cell0301 basic medicineHistone Deacetylase 2BronchiBiologyGeneral Biochemistry Genetics and Molecular BiologyChromatin remodelingProinflammatory cytokineHistonesChromatin remodelingAndrologyPulmonary Disease Chronic Obstructive03 medical and health sciencesHistone H3Western blotIL-17AmedicineHumansInterleukin 8Tiotropium BromideGeneral Pharmacology Toxicology and PharmaceuticsCells CulturedCOPDBiochemistry Genetics and Molecular Biology (all)IL-8medicine.diagnostic_testHistone deacetylase 2Chronic obstructive pulmonary diseaseAnti-Inflammatory Agents Non-SteroidalInterleukin-17Interleukin-8SmokingSputumEpithelial CellsGeneral MedicineChromatin Assembly and Disassemblymedicine.diseaserespiratory tract diseases030104 developmental biologyPharmacology Toxicology and Pharmaceutics (all)ImmunologyInterleukin 17human activitiesLife Sciences
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Carbocysteine counteracts the effects of cigarette smoke on cell growth and on the SIRT1/FoxO3 axis in bronchial epithelial cells

2016

Abstract Background Cigarette smoke may accelerate cellular senescence by increasing oxidative stress. Altered proliferation and altered expression of anti-aging factors, including SIRT1 and FoxO3, characterise cellular senescence. The effects of carbocysteine on the SIRT1/FoxO3 axis and on downstream molecular mechanisms in human bronchial epithelial cells exposed to cigarette smoke are largely unknown. Aims Aim of this study was to explore whether carbocysteine modulated SIRT1/FoxO3 axis, and downstream molecular mechanisms associated to cellular senescence, in a bronchial epithelial cell line (16-HBE) exposed to cigarette smoke. Methods 16HBE cells were stimulated with/without cigarette …

Bronchial epithelial cell0301 basic medicineSenescenceAgingPathologymedicine.medical_specialtyApoptosisSettore MED/10 - Malattie Dell'Apparato RespiratorioBiologyBiochemistryCell LineFlow cytometry03 medical and health sciencesSIRT10302 clinical medicineEndocrinologyGeneticSirtuin 1Western blotSmokeTobaccoSurvivinGeneticsmedicineHumansClonogenic assayMolecular BiologyCellular SenescenceCell ProliferationRegulation of gene expressionmedicine.diagnostic_testCell growthCarbocysteineForkhead Box Protein O3Cigarette smokeEpithelial CellsCarbocysteineCell BiologyCell biologyOxidative Stress030104 developmental biology030220 oncology & carcinogenesisFoxO3Experimental Gerontology
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Cigarette smoke alters IL-33 expression and release in airway epithelial cells

2014

AbstractAirway epithelium is a regulator of innate immune responses to a variety of insults including cigarette smoke. Cigarette smoke alters the expression and the activation of Toll Like Receptor 4 (TLR4), an innate immunity receptor. IL-33, an alarmin, increases innate immunity Th2 responses. The aims of this study were to explore whether mini-bronchoalveolar lavage (mini-BAL) or sera from smokers have altered concentrations of IL-33 and whether cigarette smoke extracts (CSE) alter both intracellular expression (mRNA and protein) and release of IL-33 in bronchial epithelial cells. The role of TLR4 in the expression of IL-33 was also explored.Mini-BALs, but not sera, from smokers show red…

Bronchial epithelial cellLipopolysaccharidesBlotting WesternBronchiInflammationRespiratory MucosaBiologyReal-Time Polymerase Chain ReactionBronchoalveolar LavageImmunoenzyme TechniquesBronchial epithelial cell; COPD; Cigarette smoke; IL-33; InflammationSmokeacute lung injury cigarette smokeinterleukin 33medicineCOPDHumansRNA MessengerReceptorMolecular BiologyCells CulturedCell ProliferationInflammationToll-like receptorInnate immune systemReverse Transcriptase Polymerase Chain ReactionInterleukinsCigarette smokeFlow CytometryInterleukin-33Immunity Innaterespiratory tract diseasesCell biologyToll-Like Receptor 4Interleukin 33ImmunologyIL-33TLR4Molecular MedicineRespiratory epitheliummedicine.symptomIntracellularBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Effects of antioxidants on CSE-induced cell death in human asthmatic primary bronchial epithelial cells

2010

The link between cigarette smoke (CS) and lung inflammation is quite strong, however relatively little is still known on the effects of CS on human bronchial epithelial cells survival during asthma. In this study we focused our attention on the apoptotic effects of CS on healthy (HC) and asthmatic (AS) primary bronchial epithelial cells (PBEC) and on the role of antioxidants to protect epithelial cells from CSE-induced apoptosis. Twenty subjects (10 HC and 10 AS) were recruited for this study and PBEC were obtained by bronchoscopy. PBEC were treated with oxidants (H2O), anti-oxidants (GSH and AA) and cigarette smoke extracts (CSE). Early apoptosis (EA) and necrosis were measured by flow cyt…

Bronchial epithelium; asthma; cigarette smoke; oxidative stressbronchial epithelial cells
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Multiple in vitro and in vivo regulatory effects of budesonide in CD4+ T lymphocyte subpopulations of allergic asthmatics.

2012

Abstract BACKGROUND: Increased activation and increased survival of T lymphocytes characterise bronchial asthma. OBJECTIVES: In this study the effect of budesonide on T cell survival, on inducible co-stimulator T cells (ICOS), on Foxp3 and on IL-10 molecules in T lymphocyte sub-populations was assessed. METHODS: Cell survival (by annexin V binding) and ICOS in total lymphocytes, in CD4+/CD25+ and in CD4+/CD25- and Foxp3 and IL-10 in CD4+/CD25+ and in CD4+/CD25-cells was evaluated, by cytofluorimetric analysis, in mild intermittent asthmatics (n = 19) and in controls (n = 15). Allergen induced T lymphocyte proliferation and the in vivo effects of budesonide in mild persistent asthmatics (n =…

BudesonideCD4-Positive T-LymphocytesMalePulmonologylcsh:Medicineimmune system diseasesT-Lymphocyte SubsetsMolecular Cell Biologylcsh:ScienceBudesonidecigarette smoke airway epithelial cells reactive oxygen species.MultidisciplinaryT CellsAllergy and HypersensitivityClinical Pharmacologyhemic and immune systemsForkhead Transcription Factorsrespiratory systemMiddle AgedFlow CytometryBronchodilator AgentsInterleukin-10Interleukin 10MedicineFemalemedicine.drugResearch ArticleAdultDrugs and DevicesAdolescentCell SurvivalImmune CellsImmunologychemical and pharmacologic phenomenaInducible T-Cell Co-Stimulator ProteinImmunomodulationIn vivomedicineHumansInducible T-Cell Co-Stimulator ProteinBiologyAsthmaCell Proliferationbusiness.industrylcsh:RT lymphocytemedicine.diseaseIn vitroAsthmarespiratory tract diseasesApoptosisImmunologylcsh:QClinical ImmunologybusinessCytometryPloS one
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Effects of cigarette smoke in tissue-engineered human bronchial mucosa: new insights on COPD pathogenesis.

2012

COPD pathogenesis.smokeSettore BIO/16 - Anatomia Umanahuman bronchial mucosatissue-engineered
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Expression of versican in large and small airways and parenchima in lungs of non-smokers smokers and COPD patients

2009

COPD Smokerssmall airwaySettore MED/10 - Malattie Dell'Apparato Respiratorio
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A Study of the Effect of Proinflammatory Cytokines on the Epithelial Cells of Smokers, With or Without COPD

2011

Introduction: Cigarette smoke is the main cause of inflammation in COPD. The mechanisms that differentiate smokers who develop COPD are diverse. In this study, we analyzed the presence of cytokines in the respiratory secretions of smokers with or without COPD and the secretory properties of the differentiated bronchial epithelium obtained from the individuals themselves after exposure to tobacco smoke. Material and methods: Twenty-seven smokers were studied, 12 of whom had COPD that had not been previously treated with steroids. In 11, samples were obtained by means of induced sputum, and the remaining samples were collected from bronchial aspiration after bronchoscopy. Concentrations of IL…

COPDPathologymedicine.medical_specialtymedicine.diagnostic_testbusiness.industryInflammationGeneral Medicinemedicine.diseaseGastroenterologyTobacco smokerespiratory tract diseasesProinflammatory cytokineBronchoscopyInternal medicinemedicineTumor necrosis factor alphaInterleukin 8Respiratory systemmedicine.symptombusinessArchivos de Bronconeumología (English Edition)
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