0000000000115808

AUTHOR

Paola Dino

0000-0001-6292-8662

showing 7 related works from this author

Notch-1 decreased expression contributes to leptin receptor downregulation in nasal epithelium from allergic turbinates

2019

Abstract BACKGROUND: Allergic rhinitis is characterized by a remodeling of nasal epithelium. Since the Notch and TGF-β signaling pathways are known to be involved in cell differentiation and remodeling processes and leptin adipokine has already been identified as a marker for homeostasis in human bronchial and nasal epithelial cells of asthmatics, roles played by these pathways have been investigated for chronic allergic rhinitis. METHODS: The leptin/leptin receptor expression has been investigated in a study with 40 biopsies from allergic (AR, n = 18) and non-allergic (C, n = 22) inferior turbinates, using immunohistochemistry, immunofluorescence staining and RT-PCR. In addition, extracts …

0301 basic medicineAdultLeptinMalemedicine.medical_specialtyBiopsyPrimary Cell CultureAdipokineTurbinatesCell LineTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineDownregulation and upregulationInternal medicinemedicineHomeostasisHumansRNA MessengerReceptor Notch1610 Medicine & healthReceptorMolecular BiologyNotch 1Leptin receptorChemistryLeptindigestive oral and skin physiologyEpithelial CellsMiddle AgedRhinitis AllergicAllergic rhinitis Epithelium Leptin NotchEpitheliumNasal Mucosa030104 developmental biologyEndocrinologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisCase-Control StudiesMolecular MedicineReceptors LeptinFemaleSignal transductionSignal Transduction
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Leptin and TGF-β1 Downregulate PREP1 Expression in Human Adipose-Derived Mesenchymal Stem Cells and Mature Adipocytes

2021

International audience; Adipose tissue is widely recognized as an extremely active endocrine organ producing adipokines as leptin that bridge metabolism and the immune system. Pre-B-cell leukemia homeobox (Pbx)-regulating protein-1 (PREP1) is a ubiquitous homeodomain transcription factor involved in the adipogenic differentiation and insulin-sensitivity processes. Leptin, as pleiotropic adipokine, and TGF-β, known to be expressed by primary pre-adipocytes [adipose-derived stem cells (ASCs)] and mature differentiated adipocytes, modulate inflammatory responses. We aimed to assess for the first time if leptin and TGF-β interfere with PREP1 expression in both ASCs and mature differentiated adi…

0301 basic medicinePREP1QH301-705.5adipocytes[SDV]Life Sciences [q-bio]Adipose tissueAdipokine030209 endocrinology & metabolism610 Medicine & healthBiologyadipocyteleptinTGF-beta1Cell and Developmental Biology03 medical and health sciences0302 clinical medicineDownregulation and upregulationTLR4Biology (General)610 Medicine & healthReceptorOriginal ResearchLeptinMesenchymal stem cellCell BiologyCell biologyadipose tissueimmune system030104 developmental biologyadipocyte-derived stem cellsAdipogenesisStem celladipocyte-derived stem cellDevelopmental Biology
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Cigarette smoke promotes inflammasome‐independent activation of caspase‐1 and ‐4 leading to gasdermin D cleavage in human macrophages

2022

Mechanisms and consequences of gasdermin D (GSDMD) activation in cigarette smoke (CS)-associated inflammation and lung disease are unknown. GSDMD is a downstream effector of caspase-1, -8, and -4. Upon cleavage, GSDMD generates pores into cell membranes. Different degrees of GSDMD activation are associated with a range of physiological outputs ranging from cell hyperactivation to pyroptosis. We have previously reported that in human monocyte-derived macrophages CS extract (CSE) inhibits the NLRP3 inflammasome and shifts the response to lipopolysaccharide (LPS) towards the TLR4-TRIF axis leading to activation of caspase-8, which, in turn, activates caspase-1. In the present work, we investig…

InflammationLipopolysaccharidesPore Forming Cytotoxic Proteinsalveolar macrophages caspasecigarette smoke inflammasome lung Caspase 1 Caspases Caspases Initiator Humans Inflammation Intracellular Signaling Peptides and Proteins Lipopolysaccharides Lipopolysaccharides NLR Family Pyrin Domain-Containing 3 Protein Phosphate-Binding Proteins Pore Forming Cytotoxic Proteins Tobacco Cigarette Smoking Inflammasomes.InflammasomesSettore BIO/16 - Anatomia UmanaMacrophagesCaspase 1Intracellular Signaling Peptides and ProteinsPhosphate-Binding ProteinsBiochemistryCaspases InitiatorCigarette SmokingCaspasesNLR Family Pyrin Domain-Containing 3 ProteinTobaccoGeneticsHumansMolecular BiologyBiotechnologyThe FASEB Journal
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Ceftaroline modulates the innate immune and host defense responses of immunocompetent cells exposed to cigarette smoke.

2017

Abstract Background Cigarette smoke, the principal risk factor for chronic obstructive pulmonary disease (COPD), negatively influences the effectiveness of the immune system’s response to a pathogen. The antibiotic ceftaroline exerts immune-modulatory effects in bronchial epithelial cells exposed to cigarette smoke. Aims and methods The present study aims to assess the effects of ceftaroline on TLR2 and TLR4 expression, LPS binding and TNF-α and human beta defensin (HBD2) release in an undifferentiated and PMA-differentiated human monocyte cell line (THP-1) exposed or not to cigarette smoke extracts (CSE). TLR2, TLR4, and LPS binding were assessed by flow cytometry, TNF-α and HBD2 release w…

0301 basic medicineLipopolysaccharidesbeta-DefensinsCell SurvivalCephalosporinLipopolysaccharideToxicologyMonocytes03 medical and health sciencesImmunologic Factor0302 clinical medicineImmune systemCell Line TumorSmokeAnti-Bacterial AgentmedicineHumansImmunologic FactorsInnate immune systemImmunocompetent cellDose-Response Relationship Drugbusiness.industryTumor Necrosis Factor-alphaMonocyteMacrophagesSmokingAntibioticCigarette smokeGeneral MedicineImmunity InnateToll-Like Receptor 2Anti-Bacterial AgentsCephalosporinsHost-Pathogen InteractionToll-Like Receptor 4TLR2030104 developmental biologymedicine.anatomical_structureBeta defensinCell cultureImmunologyHost-Pathogen InteractionsTLR4lipids (amino acids peptides and proteins)Tumor necrosis factor alphabusinessImmunocompetence030215 immunologyToxicology letters
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Exposure to cigarette smoke extract and lipopolysaccharide modifies cytoskeleton organization in bronchial epithelial cells

2017

The integrity of the respiratory epithelium is crucial for airway homeostasis. Tobacco smoke exposure and recurrent infections of the airways play a crucial role in the progression and in the decline of the respiratory function in chronic obstructive pulmonary disease (COPD). The aim of this study was to detect differentially expressed proteins in a bronchial epithelial cell line (16-HBE) stimulated with cigarette smoke extract (CSE) and lipopolysaccharide (LPS), a constituent of gram-negative bacteria, alone and/or in combination, by using two-dimensional electrophoresis (2DE) analysis coupled with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Western blot a…

Lipopolysaccharides0301 basic medicinePulmonary and Respiratory Medicinebronchial epithelial cells; cigarette smoke; cytoskeleton; Molecular Biology; Pulmonary and Respiratory Medicine; Clinical BiochemistryProteomeLipopolysaccharideCytoskeleton organizationClinical BiochemistryRespiratory MucosaCell Line03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSmokebronchial epithelial cellHumansCigarette smokeMedicineCytoskeletonMolecular Biologybronchial epithelial cellsCytoskeletonbusiness.industrycigarette smokeTobacco smoke exposureEpithelial CellsTobacco Productsrespiratory systemrespiratory tract diseases030104 developmental biologyGene Expression Regulationchemistry030220 oncology & carcinogenesisImmunologyRespiratory epitheliumAirwaybusinessHomeostasisExperimental Lung Research
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Cellular Models and Assays to Study NLRP3 Inflammasome Biology

2020

The NLRP3 inflammasome is a multi-protein complex that initiates innate immunity responses when exposed to a wide range of stimuli, including pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). Inflammasome activation leads to the release of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 and to pyroptotic cell death. Over-activation of NLRP3 inflammasome has been associated with several chronic inflammatory diseases. A deep knowledge of NLRP3 inflammasome biology is required to better exploit its potential as therapeutic target and for the development of new selective drugs. To this purpose, in the past few years, several tools have…

Programmed cell death2019-20 coronavirus outbreakInflammasomesInterleukin-1betaReviewBiologyBiochemical assaysModels BiologicalCatalysisInflammasomelcsh:ChemistryInorganic ChemistryNLRP3NLR Family Pyrin Domain-Containing 3 ProteinPyroptosismedicineDeep knowledgeAlarminsAnimalsHumansPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyInnate immune systemintegumentary systemCell modelsPathogen-Associated Molecular Pattern MoleculesOrganic ChemistryInterleukin-18InterleukinInflammasomeGeneral MedicineBiophysical assaysImmunity InnateComputer Science ApplicationsCell biologyNLRP3 inhibitorslcsh:Biology (General)lcsh:QD1-999Mechanism of actionRead-outsmedicine.symptomInflammasome complexSignal Transductionmedicine.drugInternational Journal of Molecular 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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