Search results for "Toll-like receptor"

showing 10 items of 239 documents

Herpes virus entry mediator synergizes with Toll-like receptor mediated neutrophil inflammatory responses

2006

In microbial infections polymorphnuclear neutrophils (PMN) constitute a major part of the innate host defence, based upon their ability to rapidly accumulate in inflamed tissues and clear the site of infection from microbial pathogens by their potent effector mechanisms. The recently described transmembrane receptor herpes virus entry mediator (HVEM) is a member of the tumour necrosis factor receptor super family and is expressed on many haematopoietic cells, including T cells, B cells, natural killer cells, monocytes and PMN. Interaction of HVEM with the natural ligand LIGHT on T cells has a costimulatory effect, and increases the bactericidal activity of PMN. To further characterize the f…

Cell SurvivalNeutrophilsImmunologyInflammationBiologyLigandsCell DegranulationNeutrophil ActivationPhagocytosismedicineHumansImmunology and AllergyOpsoninCells CulturedRespiratory BurstToll-like receptorInnate immune systemEffectorInterleukin-8Toll-Like ReceptorsDegranulationOriginal ArticlesAcquired immune systemRespiratory burstCell biologyImmunologyInflammation Mediatorsmedicine.symptomReceptors Tumor Necrosis Factor Member 14Immunology
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An unconventional role for miRNA: let-7 activates Toll-like receptor 7 and causes neurodegeneration

2011

Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. We uncovered an unconventional role for the microRNA let-7, a highly abundant regulator of gene expression in the CNS, in which extracellular let-7 activates the RNA-sensing Toll-like receptor (TLR) 7 and induces neurodegeneration through neuronal TLR7. Cerebrospinal fluid (CSF) from individuals with Alzheimer’s disease contains increased amounts of let-7b, and extracellular introduction of let-7b into the CSF of wild-type mice by intrathecal injection resulted in neurodegeneration. Mice lacking TLR7 were resistant to this neurodegenerative effect, but thi…

Cell signalingApoptosisElectrophoretic Mobility Shift AssayBiologyReal-Time Polymerase Chain ReactionMiceAlzheimer DiseasemicroRNAExtracellularmedicineAnimalsHumansReceptorIn Situ HybridizationMice KnockoutNeuronsToll-like receptorMembrane GlycoproteinsMicroscopy ConfocalInnate immune systemGeneral NeuroscienceNeurodegenerationBrainvirus diseasesTLR7medicine.diseaseImmunohistochemistryMice Inbred C57BLMicroRNAsHEK293 CellsToll-Like Receptor 7Nerve DegenerationCancer researchSignal TransductionNature Neuroscience
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Distinct Signaling Cascades of TREM-1, TLR and NLR in Neutrophils and Monocytic Cells

2013

Triggering receptor expressed on myeloid cells 1 (TREM-1) is an important mediator of innate inflammatory responses in microbial infections and sepsis. TREM-1 ligation on neutrophils (PMN) or monocytes results in the production of proinflammatory cytokines. Engagement of TREM-1 induces the activation of MAP kinases as well as rapid Ca<sup>2+</sup> mobilization. However, a detailed understanding of TREM-1 signaling pathways is currently lacking. We evaluated the TREM-1 signaling hierarchy in monocytic cells and found that the acute myeloid leukemia cell line MUTZ-3 expresses TREM-1 in a natural and functional manner. We compared essential signaling molecules of the TREM-1, TLR an…

Cell signalingMyeloidNeutrophilsp38 Mitogen-Activated Protein KinasesMonocytesProinflammatory cytokinePhosphatidylinositol 3-KinasesCell Line TumormedicineHumansImmunology and AllergyCalcium SignalingReceptors ImmunologicExtracellular Signal-Regulated MAP KinasesPI3K/AKT/mTOR pathwayCalcium signalingMembrane GlycoproteinsChemistryToll-Like ReceptorsMyeloid leukemiaImmunity InnateTriggering Receptor Expressed on Myeloid Cells-1Cell biologyLeukemia Myeloid Acutemedicine.anatomical_structureOrgan SpecificityCell cultureImmunologyCytokinesInflammation MediatorsSignal transductionResearch ArticleJournal of Innate Immunity
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Procoagulant activity during viral infections.

2017

The abundance of evidence suggest that inflammation of immune and non-immune cells may lead to an imbalance of the pro- and anti-coagulant state during viral infections. During systemic infections, the endothelium plays a critical role in regulating hemostasis, and severe imbalances of endothelial function and activation can contribute to organ failure. Viral infections may elevate plasma levels of procoagulant markers such as TAT and D-dimer TF-positive MPs as well as von Willebrand factor (vWF). Although multiple clinical studies are showing the association of viral infection and increased prothrombotic risk, the pathological mechanisms have not been fully identified for most viral infect…

Cell typeEndotheliumInflammation030204 cardiovascular system & hematologyThromboplastin03 medical and health sciences0302 clinical medicineImmune systemVon Willebrand factorvon Willebrand FactormedicineAnimalsHumansReceptorBlood CoagulationHemostasisbiologybusiness.industryToll-Like ReceptorsBlood Coagulation Factorsmedicine.anatomical_structureCoagulationVirus DiseasesHemostasisImmunologybiology.proteinmedicine.symptombusiness030217 neurology & neurosurgeryBiomarkersFrontiers in bioscience (Landmark edition)
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Toll-like receptor 2 is dispensable for acquired host immune resistance to Candida albicans in a murine model of disseminated candidiasis

2004

Previous work by our group showed that Toll-like receptor 2 (TLR2) is essential for activation of innate immunity, playing a major role in the response of macrophages to Candida albicans, triggering cytokine and chemokine expression, and therefore TLR2 -/- mice are more susceptible to systemic primary candidiasis. In this work, we used a murine model of systemic C. albicans infection, in which resistance to reinfection with virulent wild-type cells is induced by prior exposure of mice to a low-virulence agerminative strain of C. albicans (primary sublethal infection), to study the influence of TLR2 gene deletion on (i) the ability to develop an acquired resistance upon vaccination; (ii) the…

Chemokinemedicine.medical_treatmentImmunologyReceptors Cell SurfaceMicrobiologyMicrobiologyInterferon-gammaMiceCandida albicansmedicineAnimalsCandida albicansAntibodies FungalMice KnockoutToll-like receptorMembrane GlycoproteinsInnate immune systembiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisbiology.organism_classificationDisseminated CandidiasisInterleukin-12Immunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLTLR2Infectious DiseasesCytokineImmunoglobulin GImmunologybiology.proteinCytokinesMicrobes and Infection
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Toll-like receptor-2 is essential in murine defenses against Candida albicans infections

2004

In this work, we studied the role of toll-like receptor-2 (TLR2) in murine defenses against Candida albicans. TLR2-deficient mice experimentally infected intraperitoneally (i.p.) or intravenously (i.v.) in vivo had very significant impaired survival compared with that of control mice. In vitro production of TNF-alpha and macrophage inhibitory protein-2 (MIP-2) by macrophages from TLR2-/- mice in response to yeasts and hyphae of C. albicans were significantly lower (80% and 40%, respectively; P <0.05) than production by macrophages from wild-type mice. This impaired production of TNF-alpha and MIP-2 probably contributed to the 41% decreased recruitment of neutrophils to the peritoneal cavity…

Chemokinemedicine.medical_treatmentPhagocytosisChemokine CXCL2ImmunologyHyphaeCell CountReceptors Cell SurfaceMicrobiologyMicrobiologyMicePhagocytosisIn vivoCandida albicansmedicineAnimalsMacrophageCandida albicansCells CulturedMice KnockoutToll-like receptorMembrane GlycoproteinsbiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisFlow Cytometrybiology.organism_classificationImmunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLDisease Models AnimalInfectious DiseasesCytokineMacrophages Peritonealbiology.proteinChemokinesReactive Oxygen SpeciesMicrobes and Infection
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TLR3-induced activation of mast cells modulates CD8+ T-cell recruitment.

2005

AbstractMast cells play an important role in host defense against various pathogens, but their role in viral infection has not been clarified in detail. dsRNA, synthesized by various types of viruses and mimicked by polyinosinic-polycytidylic acid (poly(I:C)) is recognized by Toll-like receptor 3 (TLR3). In this study, we demonstrate that poly(I:C) injection in vivo potently stimulates peritoneal mast cells to up-regulate a number of different costimulatory molecules. Therefore, we examined the expression and the functional significance of TLR3 activation in mast cells. Mast cells express TLR3 on the cell surface and intracellularly. After stimulation of mast cells with poly(I:C) and Newcas…

Chemokinevirusesmedicine.medical_treatmentImmunologyNewcastle disease virusReceptors Cell SurfaceBiologyCD8-Positive T-LymphocytesBiochemistryMicemedicineCytotoxic T cellAnimalsMast CellsPhosphorylationPeritoneal CavityMice KnockoutInnate immune systemMembrane GlycoproteinsToll-Like ReceptorsCell BiologyHematologymedicine.diseaseMast cellImmunity InnateCell biologyToll-Like Receptor 3Up-RegulationMice Inbred C57BLChemotaxis Leukocytemedicine.anatomical_structureCytokinePoly I-CTLR3ImmunologyMast cell sarcomabiology.proteinCytokinesCD8Blood
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Toll-like receptors are part of the innate immune defense system of sponges (demospongiae: Porifera).

2006

During evolution and with the emergence of multicellular animals, the need arose to ward off foreign organisms that threaten the integrity of the animal body. Among many different receptors that participate in the recognition of microbial invaders, toll-like receptors (TLRs) play an essential role in mediating the innate immune response. After binding distinct microbial components, TLRs activate intracellular signaling cascades that result in an induced expression of diverse antimicrobial molecules. Because sponges (phylum Porifera) are filter feeders, they are abundantly exposed to microorganisms that represent a potential threat. Here, we describe the identification, cloning, and deduced …

CroatiaMolecular Sequence Datachemistry.chemical_compoundGeneticsAnimalsCluster AnalysisAmino Acid SequenceReceptorMolecular BiologyEcology Evolution Behavior and SystematicsIn Situ HybridizationPhylogenyDeath domainDNA PrimersToll-like receptorInnate immune systembiologyBase SequenceEffectorToll-Like ReceptorsLipopeptideSequence Analysis DNAbiology.organism_classificationBlotting NorthernImmunohistochemistryImmunity InnateCell biologyPoriferaSuberites domunculaInterleukin-1 Receptor-Associated KinaseschemistryCaspasesImmunologySignal transductionMolecular biology and evolution
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Carbocysteine regulates innate immune responses and senescence processes in cigarette smoke stimulated bronchial epithelial cells

2013

Cigarette smoke represents the major risk factor for chronic obstructive pulmonary disease (COPD). Cigarette smoke extracts (CSE) alter TLR4 expression and activation in bronchial epithelial cells. Carbocysteine, an anti-oxidant and mucolytic agent, is effective in reducing the severity and the rate of exacerbations in COPD patients. The effects of carbocysteine on TLR4 expression and on the TLR4 activation downstream events are largely unknown. This study was aimed to explore whether carbocysteine, in a human bronchial epithelial cell line (16-HBE), counteracted some pro-inflammatory CSE-mediated effects. In particular, TLR4 expression, LPS binding, p21 (a senescence marker), IL-8 mRNA and…

Cyclin-Dependent Kinase Inhibitor p21AgingNeutrophilsPhalloidinAnti-Inflammatory AgentsApoptosisBronchiInflammationBiologyToxicologySettore BIO/09 - FisiologiaAntioxidantsFlow cytometryPulmonary Disease Chronic Obstructivechemistry.chemical_compoundmedicineHumansRNA Messengersenescencebronchial cellscigaretteInnate immune systemmedicine.diagnostic_testCarbocysteineInterleukin-8SmokingEpithelial CellsCell migrationChemotaxisCarbocysteineGeneral MedicineFlow CytometryImmunity InnateCell biologyToll-Like Receptor 4chemistryImmunologyTLR4medicine.symptomInterleukin-1Signal TransductionToxicology Letters
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Roflumilast improves corticosteroid resistance COPD bronchial epithelial cells stimulated with toll like receptor 3 agonist

2015

Chronic obstructive pulmonary disease (COPD) is characterised by chronic pulmonary inflammation punctuated by periods of viral exacerbations. Recent evidence suggests that the combination of roflumilast with corticosteroids may improve the compromised anti-inflammatory properties of corticosteroids in COPD. We analyzed differential and combination anti-inflammatory effects of dexamethasone and roflumilast N-oxide in human bronchial epithelial cells (HBECs) stimulated with viral toll like receptor (TLR) agonists. Lung tissue and HBECs were isolated from healthy (n = 15), smokers (n = 12) and smokers with COPD (15). TLR3 expression was measured in lung tissue and in HBECs. IL-8 secretion was …

CyclopropanesMaleAnti-Inflammatory AgentsDrug ResistanceAminopyridinesDexamethasonePulmonary Disease Chronic ObstructiveRoflimilastAdrenal Cortex HormonesToll like receptorsCells CulturedCOPDSmokingMiddle Agedmedicine.anatomical_structureBenzamidesCorticosteroidViral exacerbationDrug Therapy CombinationFemalePulmones - Enfermedadesmedicine.drugSignal TransductionAgonistPulmonary and Respiratory Medicinemedicine.medical_specialtymedicine.drug_classCorticosteroid resistanceBronchiInternal medicinemedicineCOPDHumansInterleukin 8DexamethasoneRoflumilastAgedLungbusiness.industryResearchInterleukin-8Epithelial CellsAparato respiratoriomedicine.diseaserespiratory tract diseasesToll-Like Receptor 3EndocrinologyPoly I-CCase-Control StudiesTLR3businessRespiratory Research
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