Search results for "Epithelial cell"

showing 10 items of 475 documents

Enteropathogenic Escherichia coli O103 from rabbit elicits actin stress fibers and focal adhesions in HeLa epithelial cells, cytopathic effects that …

1997

Escherichia coli O103, a major agent of weaned-rabbit diarrhea in Western Europe, was previously shown to produce diarrhea and attaching-and-effacing intestinal lesions in experimentally infected rabbits and to possess a homolog of the eaeA gene of enteropathogenic E. coli (EPEC). In the present study, we have shown that although negative in the fluorescent-actin staining test on HeLa cells, prototype rabbit E. coli O103 strain B10 was able to induce an original cytopathic effect (CPE) in the same interaction model. This CPE was characterized by a generalized reorganization of the actin cytoskeleton and the formation of focal adhesions on the entire surface of the target cells. These effect…

[SDV]Life Sciences [q-bio]ImmunologyMutantVirulencemedicine.disease_causeMicrobiologyMicrobiology03 medical and health sciencesCytopathogenic Effect ViralmedicineCell AdhesionEscherichia coliAnimalsHumansEnteropathogenic Escherichia coliEscherichia coliEscherichia coli InfectionsComputingMilieux_MISCELLANEOUS030304 developmental biologyCytopathic effect0303 health sciencesbiologyCell DeathVirulence030306 microbiologyEpithelial Cellsbiochemical phenomena metabolism and nutritionbiology.organism_classificationActin cytoskeletonEnterobacteriaceaeActins3. Good healthIntestines[SDV] Life Sciences [q-bio]Infectious DiseasesMutagenesisParasitologyRabbitsLocus of enterocyte effacementResearch ArticleHeLa Cells
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Candida albicans-epithelial interactions: dissecting the roles of active penetration, induced endocytosis and host factors on the infection process

2012

International audience; Candida albicans frequently causes superficial infections by invading and damaging epithelial cells, but may also cause systemic infections by penetrating through epithelial barriers. C. albicans is a remarkable pathogen because it can invade epithelial cells via two distinct mechanisms: induced endocytosis, analogous to facultative intracellular enteropathogenic bacteria, and active penetration, similar to plant pathogenic fungi. Here we investigated the contributions of the two invasion routes of C. albicans to epithelial invasion. Using selective cellular inhibition approaches and differential fluorescence microscopy, we demonstrate that induced endocytosis contri…

[SDV]Life Sciences [q-bio]lcsh:MedicineYeast and Fungal ModelsPathogenesisCandidiasis OralMolecular Cell BiologyCandida albicanslcsh:ScienceCandida albicansPathogencandida albicans;epithelial interaction;endocytosis;infection0303 health sciencesFungal proteinMultidisciplinaryFungal DiseasesBlood Physiological PhenomenaCadherinsEndocytosisCorpus albicansepithelial interactionCell biologyHost-Pathogen InteractionInfectious Diseases[SDE]Environmental SciencesHost-Pathogen InteractionsMedicineCellular TypesSuperficial MycosesCandidalysinResearch ArticleMycologyBiologyEndocytosisMicrobiologyCell LineMicrobiologyFungal Proteins03 medical and health sciencesModel OrganismsMicroscopy Electron TransmissionCell Adhesion[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyHumansCell adhesionBiology030304 developmental biology030306 microbiologyIntracellular parasitelcsh:RFungiMouth MucosaEpithelial Cellsbiology.organism_classificationinfectionYeastlcsh:Q
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Chemically induced mouse models of intestinal inflammation

2007

Animal models of intestinal inflammation are indispensable for our understanding of the pathogenesis of Crohn disease and ulcerative colitis, the two major forms of inflammatory bowel disease in humans. Here, we provide protocols for establishing murine 2,4,6-trinitro benzene sulfonic acid (TNBS)-, oxazolone- and both acute and chronic dextran sodium sulfate (DSS) colitis, the most widely used chemically induced models of intestinal inflammation. In the former two models, colitis is induced by intrarectal administration of the covalently reactive reagents TNBS/oxazolone, which are believed to induce a T-cell-mediated response against hapten-modified autologous proteins/luminal antigens. In …

animal diseasesdigestive systemInflammatory bowel diseaseGeneral Biochemistry Genetics and Molecular BiologyPathogenesisOxazoloneMicechemistry.chemical_compoundAntigenmedicineAnimalsColitisbiologyDextran SulfateOxazoloneEpithelial CellsColitismedicine.diseaseUlcerative colitisdigestive system diseasesDisease Models AnimalTrinitrobenzenesulfonic AcidchemistryImmunologybiology.proteinAntibodyHaptenNature Protocols
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Intraflagellar transport protein 172 is essential for primary cilia formation and plays a vital role in patterning the mammalian brain

2008

AbstractIFT172, also known as Selective Lim-domain Binding protein (SLB), is a component of the intraflagellar transport (IFT) complex. In order to evaluate the biological role of the Ift172 gene, we generated a loss-of-function mutation in the mouse. The resulting Slb mutant embryos die between E12.5 and 13.0, and exhibit severe cranio-facial malformations, failure to close the cranial neural tube, holoprosencephaly, heart edema and extensive hemorrhages. Cilia outgrowth in cells of the neuroepithelium is initiated but the axonemes are severely truncated and do not contain visible microtubules. Morphological and molecular analyses revealed a global brain-patterning defect along the dorsal–…

animal structuresBody PatterningNodal ProteinSlbNodalBiologyArticleMiceFGF8Intraflagellar transportHoloprosencephalymedicineMHB boundaryAnimalsHedgehog ProteinsRNA MessengerCiliaNodeMolecular BiologyAdaptor Proteins Signal TransducingBody PatterningGeneticsMammalsCell DeathCiliumEndodermNeural tubeIntracellular Signaling Peptides and ProteinsBrainGene Expression Regulation DevelopmentalCell BiologyEmbryo MammalianCell biologyNeuroepithelial cellGastrulationCytoskeletal Proteinsmedicine.anatomical_structurePhenotypeIFT172Gene Targetingembryonic structuresNODALBiomarkersGene DeletionDevelopmental BiologySignal TransductionDevelopmental Biology
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An impaired alveolar-capillary barrier in vitro : effect of proinflammatory cytokines and consequences on nanocarrier interaction.

2009

The alveolar region of the lung is an important target for drug and gene delivery approaches. Treatment with drugs is often necessary under pathophysiological conditions, in which there is acute inflammation of the target organ. Therefore, in vitro models of the alveolar-capillary barrier, which mimic inflammatory conditions in the alveolar region, would be useful to analyse and predict effects of novel drugs on healthy or inflamed tissues. The epithelial cell line H441 was cultivated with primary isolated human pulmonary microvascular endothelial cells (HPMECs) or the endothelial cell line ISO-HAS-1 on opposite sides of a permeable filter support under physiological and inflammatory condi…

bilayerPathologytight junctions[SDV.BIO]Life Sciences [q-bio]/Biotechnologymedicine.medical_treatment[SDV]Life Sciences [q-bio]02 engineering and technology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]nanocarrier interactionBiochemistry[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]Electric ImpedancePolyethyleneimineBarrier function0303 health sciencesTight junctionArticlesTransfection021001 nanoscience & nanotechnologyImmunohistochemistryCell biologyEndothelial stem cellCytokine[SDV.TOX]Life Sciences [q-bio]/Toxicology0210 nano-technologyBiotechnologymedicine.medical_specialtyBiomedical EngineeringBiophysicsBioengineering[SDV.BC]Life Sciences [q-bio]/Cellular BiologyGene deliveryBiologyLung injuryModels BiologicalCell LineProinflammatory cytokineBiomaterialsInterferon-gamma03 medical and health sciencesmedicineHumanslung injury030304 developmental biologyAnalysis of VarianceTumor Necrosis Factor-alphaEndothelial CellsBiological TransportCoculture Techniquesalveolar-capillary barrierAlveolar Epithelial CellsNanoparticles
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Cytotoxicity of the Urokinase-Plasminogen Activator Inhibitor Carbamimidothioic Acid (4-Boronophenyl) Methyl Ester Hydrobromide (BC-11) on Triple-Neg…

2015

BC-11 is an easily synthesized simple thiouronium-substituted phenylboronic acid, which has been shown to be cytotoxic on triple negative MDA-MB231 breast cancer cells by inducing a perturbation of cell cycle when administered at a concentration equal to its ED50 at 72 h (117 μM). Exposure of cells to BC-11, either pre-absorbed with a soluble preparation of the N-terminal fragment of urokinase-plasminogen activator (uPa), or in co-treatment with two different EGFR inhibitors, indicated that: (i) BC-11 acts via binding to the N-terminus of the enzyme where uPa- and EGF receptor-recognizing sites are present, thereby abrogating the growth-sustaining effect resulting from receptor binding

boronic acidPharmaceutical ScienceGene ExpressionApoptosisAnalytical ChemistryDrug DiscoveryCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaCytotoxicityEGFR inhibitorschemistry.chemical_classificationCell CycleDrug SynergismCell cycleBoronic AcidsMitochondriaErbB ReceptorsBiochemistryChemistry (miscellaneous)Molecular MedicinecytotoxicityFemaleQD0241Antineoplastic AgentsArticlelcsh:QD241-441plasminogen activator inhibitorbreast cancerlcsh:Organic chemistryCell Line TumorHumansPhysical and Theoretical ChemistryMammary Glands HumanCell ProliferationQD0415Reactive oxygen speciesHydrobromideOrganic ChemistryEpithelial CellsBC-11Molecular biologyUrokinase-Type Plasminogen ActivatorPlasminogen InactivatorsEnzymechemistryApoptosisQuinazolinesMDA-MB231 cellsReactive Oxygen Speciesboronic acid; BC-11; plasminogen activator inhibitor; breast cancer; cytotoxicity; MDA-MB231 cellsMolecules
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Sildenafil protects human mammary epithelial cells against ROS production induced by estradiol

2010

Several studies suggest that xanthine dehydrogenase (XDH) and its oxidase form (XO) play an important role in various types of ischemic and vascular injuries. Recently, we have demonstrated that estradiol (E2) induces a significant decrease of the expression and activity of XDH and of its conversion to XO in human mammary epithelial cells. E2 is known to induce upregulation of eNOS gene expression in aortic endothelial cells. Because the XO-derived O2·- combines with ·NO to yield ONOO-, and considering that ONOO- converts XDH to XO, the resulting increase of XO activity and reactive oxygen species production would eventually lead to a further increase of ONOO- production, thus creating a vi…

chemistry.chemical_classificationOxidase testmedicine.medical_specialtyReactive oxygen speciesNADPH oxidasebiologyEndocrinology Diabetes and MetabolismPhosphodiesteraseGeneral Medicinemedicine.disease_causeMolecular biologyEndocrinologyEnzymeEndocrinologyDownregulation and upregulationchemistryXanthine dehydrogenaseSettore BIO/10 - BiochimicaInternal medicinemedicinebiology.proteinMolecular BiologyOxidative stressestradiol (E2) human mammaty epithelial cells (HMECs) oxidative stress inhibition reactive oxygen species (ROS) production sildenafil xanthine dehydrogenase (XDH) xanthine oxidase (XO).Hormone Molecular Biology and Clinical Investigation
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Electrochemical sensor for evaluating oxidative stress in airway epithelial cells

2021

Cigarette smoke exposure induces oxidative stress within the airways. Increased oxidative burden contributes to the pathogenesis of chronic lung disorders and is associated with aging and chronic inflammation. Airway epithelial cells highly contribute to Reactive Oxygen Species (ROS) generation within injured and inflamed lung tissues. Among ROS, hydrogen peroxide (H2O2) can be monitored in the extracellular space. Herein, we present an amperometric/voltammetric sensor based on gold nanoparticles and graphene oxide able to detect H2O2 with good sensitivity and selectivity. Using this sensor, H2O2 release was measured in conditioned medium from primary bronchial epithelial cells (PBEC), bron…

chemistry.chemical_classificationReactive oxygen speciesmedicine.diagnostic_testbusiness.industrySmokingelectrochemical sensorsInflammationhydrogen peroxideOxidative phosphorylationResveratrolmedicine.disease_causeCell biologyFlow cytometryEpithelial cellchemistry.chemical_compoundSettore ING-IND/23 - Chimica Fisica ApplicatachemistrySettore ING-IND/17 - Impianti Industriali MeccaniciExtracellularMedicinemedicine.symptombusinessOxidative stressIntracellular
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Cigarette smoke increases TLR4 and modifies LPS mediated responses in airway epithelial cells.

2008

Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke. The main goal of this study was to explore the effects of cigarette smoke extracts (CSE) on Tolllike receptor (TLR) expression and activation in a human bronchial epithelial cell line (16-HBE). The CSE increased the expression of TLR4 and the lipopolysaccharide (LPS) binding, the nuclear factor-jB (NF-jB) activation, the release of interleukin-8 (IL-8) and the chemotactic activity toward neutrophils. It did not induce TLR2 expression or extracellular signal-regulated signal kinase 1/2 (ERK1/2) activation. The LPS increased the expression of TLR4 and induced both NF-jB a…

cigarette smokeSettore MED/10 - Malattie Dell'Apparato Respiratorioairway epithelial cellToll-like receptors
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Roflumilast N-oxide, a PDE4 inhibitor, improves cilia motility and ciliated human bronchial epithelial cells compromised by cigarette smoke in vitro

2012

BACKGROUND AND PURPOSEMucociliary malfunction occurs in chronic obstructive pulmonary disease (COPD) and compromised functions of ciliated bronchial epithelial cells may contribute to this. Cigarette smoke, a major risk factor for COPD, impairs ciliary beat frequency (CBF). cAMP augments CBF. This in vitro study addressed, in differentiated, primary human bronchial epithelial cells, whether roflumilast N-oxide, a PDE4 inhibitor, (i) augments CBF; (ii) prevents the reduction in CBF induced by cigarette smoke extract (CSE); and (iii) protects against the loss of the ciliated phenotype following long-term CSE exposure.EXPERIMENTAL APPROACHAir-liquid interface cultured human bronchial epithelia…

ciliary motilityroflumilastbronchial epithelial cellsphosphodiesterase-4
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