Search results for "Toll-Like Receptor 4"

showing 10 items of 92 documents

A role for Toll-like receptor mediated signals in neutrophils in the pathogenesis of the anti-phospholipid syndrome.

2012

The anti-phospholipid syndrome (APS) is characterized by recurrent thrombosis and occurrence of anti-phospholipid antibodies (aPL). aPL are necessary, but not sufficient for the clinical manifestations of APS. Growing evidence suggests a role of innate immune cells, in particular polymorphonuclear neutrophils (PMN) and Toll-like receptors (TLR) to be additionally involved. aPL activate endothelial cells and monocytes through a TLR4-dependent signalling pathway. Whether this is also relevant for PMN in a similar way is currently not known. To address this issue, we used purified PMN from healthy donors and stimulated them in the presence or absence of human monoclonal aPL and the TLR4 agonis…

LipopolysaccharidesNeutrophilsImmunology610 MedizinImmunoglobulinslcsh:MedicineInflammationApoptosisImmunopathologyBiologyNeutrophil ActivationAutoimmune DiseasesPhagocytosisimmune system diseases610 Medical sciencesmedicineHumansInterleukin 8L-SelectinReceptorlcsh:ScienceBiologyImmune ResponseneoplasmsRespiratory BurstInflammationToll-like receptorMultidisciplinaryInnate immune systemCD11b AntigenCoagulation DisordersEffectorInterleukin-8lcsh:RImmunityHematologyAntiphospholipid SyndromeFlow CytometryInnate ImmunityRespiratory burstToll-Like Receptor 4ImmunologyTLR4MedicineClinical Immunologylcsh:Qmedicine.symptomResearch ArticleSignal TransductionPLoS ONE
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Nanoscale distribution of TLR4 on primary human macrophages stimulated with LPS and ATI

2019

Toll-like receptor 4 (TLR4) plays a crucial role in the recognition of invading pathogens. Upon activation by lipopolysaccharides (LPS), TLR4 is recruited into specific membrane domains and dimerizes. In addition to LPS, TLR4 can be stimulated by wheat amylase-trypsin inhibitors (ATI). ATI are proteins associated with gluten containing grains, whose ingestion promotes intestinal and extraintestinal inflammation. However, the effect of ATI vs. LPS on the membrane distribution of TLR4 at the nanoscale has not been analyzed. In this study, we investigated the effect of LPS and ATI stimulation on the membrane distribution of TLR4 in primary human macrophages using single molecule localization m…

LipopolysaccharidesSingle molecule localizationStimulationInflammation02 engineering and technology010402 general chemistry01 natural sciencesmedicineHumansDistribution (pharmacology)General Materials ScienceReceptorCells CulturedChemistryMacrophagesCell Membrane021001 nanoscience & nanotechnology0104 chemical sciencesCell biologyToll-Like Receptor 4MembraneMicroscopy FluorescenceTLR4lipids (amino acids peptides and proteins)Receptor clusteringmedicine.symptomTrypsin Inhibitors0210 nano-technologyNanoscale
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Cilomilast counteracts the effects of cigarette smoke in airway epithelial cells.

2010

Abstract Cigarette smoke extracts (CSE) alter TLR4 expression and activation in bronchial epithelial cells. Cilomilast, a phosphodiesterase-4 inhibitor, inhibits cigarette smoke-induced neutrophilia. This study was aimed to explore whether cilomilast, in a human bronchial epithelial cell line (16-HBE), counteracted CSE effects. In particular, TLR4 expression, IP-10 and IL-8 release, lymphocyte and neutrophil chemotactic activity and ERK and IkBa phosphorylation in CSE and LPS-stimulated 16-HBE were assessed. CSE increased TLR4 expression, reduced IP-10 release and lymphocyte chemotactic activity and increased IL-8 release and neutrophil chemotactic activity. Cilomilast reduced TLR4 expressi…

MAPK/ERK pathwayCyclohexanecarboxylic AcidsLymphocyteImmunologyCyclohexanecarboxylic AcidRespiratory MucosaBiologyCell LineSmokeparasitic diseasesNitrilesmedicineHumansLymphocytesCOPDChemotaxisCilomilastInterleukin-8ChemotaxiChemotaxisTobacco Use Disordermedicine.diseaseNeutrophiliaChemokine CXCL10Toll-Like Receptor 4medicine.anatomical_structureGene Expression RegulationPhosphodiesterase 4 InhibitorImmunologyTLR4PhosphorylationLymphocytePhosphodiesterase 4 Inhibitorsmedicine.symptomNitrileHumanmedicine.drugSignal TransductionCellular immunology
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Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-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 Toll-like 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-kappaB (NF-kappaB) 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 bot…

MAPK/ERK pathwayLipopolysaccharidesLipopolysaccharideNeutrophilsImmunologyBronchiRespiratory Mucosachemistry.chemical_compoundSmokeTobaccoImmunology and AllergyHumansImmunity MucosalCell Line TransformedMitogen-Activated Protein Kinase 1Toll-like receptorMitogen-Activated Protein Kinase 3Interleukin-8NF-kappa BChemotaxisEpithelial CellsOriginal ArticlesCell biologyChemokine CXCL10Toll-Like Receptor 4TLR2Chemotaxis LeukocytechemistryImmunologyTLR4Respiratory epitheliumSignal transductionSignal TransductionImmunology
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TLR4 elimination prevents synaptic and myelin alterations and long-term cognitive dysfunctions in adolescent mice with intermittent ethanol treatment.

2015

The adolescent brain undergoes important dynamic and plastic cell changes, including overproduction of axons and synapses, followed by rapid pruning along with ongoing axon myelination. These developmental changes make the adolescent brain particularly vulnerable to neurotoxic and behavioral effects of alcohol. Although the mechanisms of these effects are largely unknown, we demonstrated that ethanol by activating innate immune receptors toll-like receptor 4 (TLR4), induces neuroinflammation and brain damage in adult mice. The present study aims to evaluate whether intermittent ethanol treatment in adolescence promotes TLR4-dependent pro-inflammatory processes, leading to myelin and synapti…

MAPK/ERK pathwaySynaptic dysfunctionImmunologyNitric Oxide Synthase Type IIBrain damageHMGB1Behavioral NeuroscienceMyelinMiceCognitionmedicineAnimalsTLR4AxonHMGB1 ProteinReceptorNeuroinflammationMyelin SheathMice KnockoutMitogen-Activated Protein Kinase KinasesbiologyBinge ethanol treatmentEthanolEndocrine and Autonomic SystemsNF-kappa BCentral Nervous System DepressantsMyelin alterationsAdolescenceToll-Like Receptor 4medicine.anatomical_structureCyclooxygenase 2SynapsesTLR4biology.proteinmedicine.symptomPsychologyCognition DisordersNeuroscienceCognitive behaviorAlcohol-Related DisordersMyelin ProteinsSignal TransductionBrain, behavior, and immunity
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Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
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Deregulation of TLR4 signaling pathway characterizes Bicuspid Aortic valve syndrome

2019

AbstractBicuspid aortic valve (BAV) disease is recognized to be a syndrome with a complex and multifaceted pathophysiology. Its progression is modulated by diverse evolutionary conserved pathways, such as Notch-1 pathway. Emerging evidence is also highlighting the key role of TLR4 signaling pathway in the aortic valve pathologies and their related complications, such as sporadic ascending aorta aneurysms (AAA). Consistent with these observations, we aimed to evaluate the role of TLR4 pathway in both BAV disease and its common complication, such as AAA. To this aim, 70 subjects with BAV (M/F 50/20; mean age: 58.8 ± 14.8 years) and 70 subjects with tricuspid aortic valve (TAV) (M/F 35/35; mea…

Male0301 basic medicineAortic valveBicuspid Aortic valve syndromeHeart Valve Diseaseslcsh:MedicineDisease0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseTLR4lcsh:ScienceAortaAged 80 and overMultidisciplinarySyndromeMiddle AgedPathophysiologymedicine.anatomical_structureAortic Valvecardiovascular systemCardiologyFemaleSignal Transductionmedicine.medical_specialtyCardiologyArticleProinflammatory cytokine03 medical and health sciencesmedicine.arteryInternal medicineAscending aortamedicineHumansbicuspid valveAgedbicuspid valve; TLR4; aortic diseaseBAV TLR4 AAATumor Necrosis Factor-alphabusiness.industryInterleukinslcsh:RSettore MED/23 - Chirurgia CardiacaValvular diseaseaortic diseasemedicine.diseaseToll-Like Receptor 4030104 developmental biologyTLR4lcsh:QbusinessComplication030217 neurology & neurosurgeryScientific Reports
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Involvement of TLR4 in the long-term epigenetic changes, rewarding and anxiety effects induced by intermittent ethanol treatment in adolescence

2016

Studies in humans and experimental animals have demonstrated the vulnerability of the adolescent brain to actions of ethanol and the long-term consequences of binge drinking, including the behavioral and cognitive deficits that result from alcohol neurotoxicity, and increased risk to alcohol abuse and dependence. Although the mechanisms that participate in these effects are largely unknown, we have shown that ethanol by activating innate immune receptors, toll-like receptor 4 (TLR4), induces neuroinflammation, impairs myelin proteins and causes cognitive dysfunctions in adolescent mice. Since neuroimmune signaling is also involved in alcohol abuse, the aim of this study was to assess whethe…

Male0301 basic medicineEpigenetic changesmedia_common.quotation_subjectImmunologyRewarding effectsAlcohol abuseBinge drinkingAnxietyBinge DrinkingEpigenesis GeneticMice03 medical and health sciencesBehavioral Neuroscience0302 clinical medicineRewardNeuroimmune systemmedicineAnimalsTLR4Neuroinflammationmedia_commonMice KnockoutEthanolBinge ethanol treatmentEndocrine and Autonomic SystemsAddictionAge FactorsNeurotoxicityBrainAnxiety-like behaviormedicine.diseaseEthanol preferencePrelimbic medial prefrontal cortexAdolescenceMice Inbred C57BLToll-Like Receptor 4Alcoholism030104 developmental biologySynaptic plasticityFemaleCognition DisordersPsychologyNeuroscienceMyelin Proteins030217 neurology & neurosurgeryFOSBBrain, Behavior, and Immunity
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Critical role of TLR4 in uncovering the increased rewarding effects of cocaine and ethanol induced by social defeat in male mice

2020

Abstract Background Substance use disorders and social stress are currently associated with changes in the immune system response by which they induce a proinflammatory state in neurons and glial cells that eventually modulates the reward system. Aims The aim of the present work was to assess the role of the immune TLR4 (Toll-like receptors 4) and its signaling response in the increased contextual reinforcing effects of cocaine and reinforcing effects of ethanol (EtOH) induced by social defeat (SD) stress. Methods Adult male C57BL/6 J wild-type (WT) mice and mice deficient in TLR4 (TLR4-KO) were assigned to experimental groups according to stress condition (exploration or SD). Three weeks a…

Male0301 basic medicinemedicine.medical_specialtyHippocampusSelf AdministrationStriatumProinflammatory cytokineSocial DefeatSocial defeatMice03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineCocaineDopamine Uptake InhibitorsRewardInternal medicineConditioning PsychologicalmedicineAnimalsReceptorMice KnockoutPharmacologySocial stressEthanolbusiness.industryConditioned place preferenceMice Inbred C57BLToll-Like Receptor 4030104 developmental biologyEndocrinologyTLR4business030217 neurology & neurosurgeryNeuropharmacology
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Association between the polymorphisms of TLR4 and CD14 genes and Alzheimer's disease.

2008

Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disease which in Western society mainly accounts for clinical dementia. Inflammation plays a key role in AD and dissecting the genetics of inflammation may provide an answer to the possible treatment. Hence, the better understanding of different molecular and cellular inflammatory mechanisms is crucial for complete knowledge of AD pathophysiology, and for its prevention and drug therapy. Accordingly, in the present study we evaluated whether the pro-inflammatory polymorphisms of lipopolysaccaride-receptors, +896A/G Toll-Like Receptor (TLR4) and -260C/T CD14, are risk factors for AD. The study included both 626 AD …

MaleALZHEIMER'S DISEASEINFLAMMATIONINNATE IMMUNITYTLR4CD14Lipopolysaccharide ReceptorsInflammationSingle-nucleotide polymorphismDiseaseSystemic inflammationPolymorphism Single NucleotideSeverity of Illness IndexDegenerative diseaseINFLAMMATIONAlzheimer DiseaseRisk FactorsDrug DiscoverymedicineDementiaSNPHumansTLR4AgedPharmacologyAged 80 and overbusiness.industryMiddle Agedmedicine.diseaseToll-Like Receptor 4ItalyALZHEIMER'S DISEASEImmunologyINNATE IMMUNITYFemalemedicine.symptomAlzheimer's diseasebusinessCD14
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