Search results for "Toll-like receptor"

showing 10 items of 239 documents

Effects in cigarette smoke stimulated bronchial epithelial cells of a corticosteroid entrapped into nanostructured lipid carriers

2014

Background Nanomedicine studies have showed a great potential for drug delivery into the lung. In this manuscript nanostructured lipid carriers (NLC) containing Fluticasone propionate (FP) were prepared and their biocompatibility and effects in a human bronchial epithelial cell line (16-HBE) stimulated with cigarette smoke extracts (CSE) were tested. Results Biocompatibility studies showed that the NLC did not induce cell necrosis or apoptosis. Moreover, it was confirmed that CSE increased intracellular ROS production and TLR4 expression in bronchial epithelial cells and that FP-loaded NLC were more effective than free drug in modulating these processes. Finally, the nanoparticles increased…

BiocompatibilityCellBiomedical EngineeringMedicine (miscellaneous)Pharmaceutical ScienceApoptosisBronchiBioengineeringChronic obstructive pulmonary disease; Asthma; hronic obstructive pulmonary disease.PharmacologyFluticasone propionatemedicine.disease_causeApplied Microbiology and BiotechnologyNanostructured lipid carriers Corticosteroid Fluticasone propionate Cigarette smoke Airway epithelial cell Chronic obstructive pulmonary disease Asthmachemistry.chemical_compoundAirway epithelial cellmedicineHumansCorticosteroidCells CulturedFluticasoneDrug CarriersNanostructured lipid carriersbusiness.industryResearchChronic obstructive pulmonary diseaseSmokingCigarette smokeEpithelial CellsGlutathioneGlutathioneLipidsAsthmaNanostructuresToll-Like Receptor 4medicine.anatomical_structurechemistrySettore CHIM/09 - Farmaceutico Tecnologico ApplicativoApoptosisDrug deliveryFluticasoneMolecular MedicineReactive Oxygen SpeciesbusinessOxidative stressIntracellularmedicine.drugJournal of Nanobiotechnology
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Chronic peroxisome proliferator-activated receptorβ/δ agonist GW0742 prevents hypertension, vascular inflammatory and oxidative status, and endotheli…

2015

Endothelial dysfunction plays a key role in obesity-induced risk of cardiovascular disease. The aim of the present study was to analyze the effect of chronic peroxisome proliferator-activated receptor (PPAR)β/δ agonist GW0742 treatment on endothelial function in obese mice fed a high-fat diet (HFD).Five-week-old male mice were allocated to one of the following groups: control, control-treated (GW0742, 3 mg/kg per day, by oral gavage), HFD, HFD + GW0742, HFD + GSK0660 (1 mg/kg/day, intraperitoneal) or HFD-GW0742-GSK0660 and followed for 11 or 13 weeks. GW0742 administration to mice fed HFD prevented the gain of body weight, heart and kidney hypertrophy, and fat accumulation. The increase in …

Blood GlucoseMaleAgonistmedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumPhysiologymedicine.drug_classCaveolin 1Peroxisome proliferator-activated receptorThiophenesDiet High-FatGW0742MiceInsulin resistanceInternal medicineInternal MedicinemedicineAnimalsObesityPPAR deltaSulfonesEndothelial dysfunctionReceptorPPAR-betaAortachemistry.chemical_classificationInterleukin-6Tumor Necrosis Factor-alphabusiness.industryGlucose Tolerance TestPeroxisomemedicine.diseaseToll-Like Receptor 4VasodilationThiazolesEndocrinologymedicine.anatomical_structureAdipose TissuechemistryHypertensionAdiponectinEndothelium VascularInsulin ResistanceReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessJournal of Hypertension
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The gut microbiota: An emerging risk factor for cardiovascular and cerebrovascular disease

2018

Commensal gut microbiota have recently been implicated in cardiovascular disease (CVD) and cerebrovascular disease. Atherosclerotic plaque formation depends on the colonization status of the host. In addition to host nutrition and the related microbiota-dependent metabolic changes, activation of innate immune pathways triggers the development of atherosclerosis and supports arterial thrombosis. Gnotobiotic mouse models have uncovered that activation of Toll-like receptor-2 by gut microbial ligands supports von Willebrand factor-integrin mediated platelet deposition to the site of vascular injury. Depending on nutritional factors, the microbiota-derived choline-metabolite trimethylamine N-ox…

Blood Platelets0301 basic medicineIntegrinsEmerging riskImmunologyDiseaseBiologyGut floradigestive systemMethylaminesMice03 medical and health sciencesVon willebrandRisk Factorsvon Willebrand FactormedicineAnimalsHumansImmunology and AllergyPlateletSymbiosisInnate immune systemInfant NewbornInfantThrombosisAtherosclerosisbiology.organism_classificationmedicine.diseaseThrombosisImmunity InnatePlaque AtheroscleroticToll-Like Receptor 2Gastrointestinal MicrobiomeCerebrovascular Disorders030104 developmental biologyCardiovascular DiseasesArterial thrombusImmunologyEuropean Journal of Immunology
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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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Glycoprotein 96-activated dendritic cells induce a CD8-biased T cell response.

2005

Heat shock proteins (Hsps) are able to induce protective immune responses against pathogens and tumors after injection into immunocompetent hosts. The activation of components of the adaptive immune system, including cytotoxic T lymphocytes specific for pathogen- or tumor-derived peptides, is crucial for the establishment of immuno- protection. Hsps acquire these peptides during intracellular protein degradation and when released during necrotic cell death, facilitate their uptake and Minor Histocompatibility Complex (MHC)-restricted representation by professional antigen-presenting cells (APCs). In addition, the interaction of Hsps with APCs, including the Endoplasmatic Reticulum (ER)-resi…

CD4-Positive T-LymphocytesLipopolysaccharidesAntigen-Presenting CellsBone Marrow CellsMice TransgenicReceptors Cell SurfaceBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexLymphocyte ActivationBiochemistryMiceImmune systemHeat shock proteinCytotoxic T cellAnimalsHumansAntigen-presenting cellCells CulturedMembrane GlycoproteinsToll-Like ReceptorsCell DifferentiationCell BiologyDendritic cellDendritic CellsOriginal ArticlesAcquired immune systemLymphocyte SubsetsCell biologyMice Inbred C57BLToll-Like Receptor 4biology.proteinInflammation MediatorsCD8Signal TransductionCell stresschaperones
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TLR2 and Dectin-1 Signaling in Mouse Hematopoietic Stem and Progenitor Cells Impacts the Ability of the Antigen Presenting Cells They Produce to Acti…

2020

Microbial recognition by pattern recognition receptors (PRRs) expressed on hematopoietic stem and progenitor cells (HSPCs) not only activates myelopoiesis but also programs the function of the monocytes and macrophages they produce. For instance, changes in HSPC programming modify the ability of macrophages derived from them to produce inflammatory cytokines. While HSPCs exposed to a TLR2 agonist give rise to tolerized macrophages (lower proinflammatory cytokine production), HSPCs treated with Dectin-1 ligands produce trained macrophages (higher proinflammatory cytokine production). However, nothing is known about the impact of HSPC exposure to microbes on the function of antigen presenting…

CD4-Positive T-LymphocytesOvalbuminhematopoietic stem and progenitor cellsCD4 T cellsAntigen-Presenting CellsMice Transgenicantigen presenting cellsLymphocyte Activationinnate immune memoryProinflammatory cytokineLipopeptidesCandida albicansAnimalsTLR2Lectins C-TypeProgenitor cellAntigen-presenting celllcsh:QH301-705.5CD86CD40biologyChemistryCommunicationHistocompatibility Antigens Class IIZymosanGeneral MedicineTh1 CellsHematopoietic Stem CellsAcquired immune systemToll-Like Receptor 2Cell biologyMice Inbred C57BLlcsh:Biology (General)biology.proteinCytokinesTh17 CellsMyelopoiesisCD80Dectin-1Signal TransductionCells
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Toll-like receptors: Expression and involvement in Multiple Myeloma

2010

Multiple Myeloma (MM) cells express and respond to a broad range of TLRs. Accumulating evidences suggest that TLRs act as double-edged sword in MM biology. Indeed, TLR9 or TLR3 ligands could enhance immunity against MM cells or directly induce cell apoptosis, whereas various TLR agonists could induce MM survival, proliferation, and immune escape. This review is focused on the heterogeneous expression and function of TLRs in MM and on the potential implication of TLR ligands of infectious or endogenous origin in MM emergence, resistance, or progression.

Cancer ResearchTLR9ApoptosisEndogenyHematologyBiologyLigandsmedicine.diseaseToll-Like Receptor 3Cell biologyGene Expression Regulation NeoplasticImmune systemOncologyApoptosisImmunityToll-Like Receptor 9TLR3medicineAnimalsHumansTumor EscapeMultiple MyelomaReceptorMultiple myelomaLeukemia Research
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Pharmacogenomics: a tool to prevent and cure coronary heart disease.

2007

Inflammation and genetics play an important role in the pathogenesis of coronary heart disease (CHD). This is supported by epidemiological studies which have thoroughly investigated the association between CHD and gene polymorphisms of the inflammatory molecules. Moreover, efforts to find elective therapy have not been rewarding and, despite the increasing appreciation of the role of genetics in CHD and myocardial infarction (MI) pathogenesis, pharmacogenomic approaches to uncover drug target have not been extensively explored. A critical search of published literature has suggested few inflammatory genes directly involved in the risk to develop CHD and MI. The selected genes are, the pro- …

Candidate genepharmacogenomicLipoxygenaseLipopolysaccharide ReceptorsMyocardial InfarctionCoronary DiseaseDiseaseBioinformaticsRisk AssessmentPathogenesisRisk FactorsDrug DiscoverymedicinecytokineHumansGenetic Predisposition to DiseaseMyocardial infarctionTLR4PharmacologyInflammationPolymorphism Geneticbusiness.industryPatient SelectionCase-control studyCOXLOXmedicine.diseaseAtherosclerosisToll-Like Receptor 4Treatment OutcomePharmacogeneticsProstaglandin-Endoperoxide SynthasesPharmacogenomicsCase-Control StudiesImmunologyCytokinesReceptors ChemokineChemokinesbusinessRisk assessmentCD14CCR5PharmacogeneticsCurrent pharmaceutical design
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Toll-like receptor 3 mediates expression of clusterin/apolipoprotein J in vascular smooth muscle cells stimulated with RNA released from necrotic cel…

2010

Clusterin/Apolipoprotein J is a protein that is upregulated in a broad spectrum of diverse pathological processes. The predominant form is a secreted glycoprotein (sCLU) with cytoprotective and anti-inflammatory properties which shows enhanced expression in vascular smooth muscle cells (VSMC) following aortic injury and in atherosclerotic disease. Recent evidence indicates that during atherosclerosis, Toll-like receptors (TLRs) are activated in vascular cells by endogenous ligands. Here, we analyzed whether CLU expression in VSMC is controlled by TLRs, and stimulated by factors associated with or released by necrotic cells. Activation of TLR3 by the synthetic RNA analogue polyinosinic-polyc…

Cell ExtractsProtein DenaturationHot TemperatureMyocytes Smooth MuscleMedizinGene ExpressionBiologyTransfectionMuscle Smooth VascularCell LineMiceNecrosisDogsDownregulation and upregulationGene expressionAnimalsHumansChemokine CCL2Mice KnockoutMessenger RNAToll-like receptorClusterinToll-Like ReceptorsProteinsChloroquineCell BiologyMolecular biologyEndocytosisRatsToll-Like Receptor 3Mice Inbred C57BLTLR2Adaptor Proteins Vesicular TransportClusterinPoly I-CCulture Media ConditionedTLR3biology.proteinRNAEctopic expressionExperimental cell research
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IgG1 B cell receptor signaling is inhibited by CD22 and promotes the development of B cells whose survival is less dependent on Ig alpha/beta.

2007

We describe a mouse strain in which B cell development relies either on the expression of membrane-bound immunoglobulin (Ig) gamma1 or mu heavy chains. Progenitor cells expressing gamma1 chains from the beginning generate a peripheral B cell compartment of normal size with all subsets, but a partial block is seen at the pro- to pre-B cell transition. Accordingly, gamma1-driven B cell development is disfavored in competition with developing B cells expressing a wild-type (WT) IgH locus. However, the mutant B cells display a long half-life and accumulate in the mature B cell compartment, and even though partial truncation of the Ig alpha cytoplasmic tail compromises their development, it does…

Cell SurvivalCellular differentiationSialic Acid Binding Ig-like Lectin 2ImmunologyNaive B cellB-cell receptorImmunoglobulinsReceptors Antigen B-CellBiologyArticle03 medical and health sciencesMice0302 clinical medicinemedicineImmunology and AllergyAnimalsProgenitor cellMemory B cellB cell030304 developmental biologyCell ProliferationMice Knockout0303 health sciencesB-LymphocytesCell growthCD22Toll-Like ReceptorsCell DifferentiationArticlesMolecular biologyCell biologyMice Inbred C57BLmedicine.anatomical_structureImmunoglobulin GMutationCalciumDimerizationCD79 AntigensSpleen030215 immunologyProtein BindingSignal TransductionThe Journal of experimental medicine
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