Search results for "TLR2"

showing 10 items of 57 documents

TLR2, TLR4 and Dectin-1 signalling in hematopoietic stem and progenitor cells determines the antifungal phenotype of the macrophages they produce

2016

TLRs represent an attractive target for the stimulation of myeloid cell production by HSPCs. We have previously demonstrated that HSPCs use TLR2 to sense Candida albicans in vivo and induce the production of macrophages. In this work, we used an in vitro model of HSPCs differentiation to investigate the functional consequences for macrophages of exposure of HSPCs to various PAMPs and C. albicans cells. Mouse HSPCs (Lin(-) cells) were cultured with M-CSF to induce macrophage differentiation, in the presence or absence of the following PRR agonists: Pam3CSK4 (TLR2 ligand), LPS (TLR4 ligand), depleted zymosan (which only activates Dectin-1), or C. albicans yeasts (which activate several PRRs, …

Lipopolysaccharides0301 basic medicineMacrophage colony-stimulating factorCellular differentiationImmunologyBiologyMicrobiologyMicrobiologyProinflammatory cytokineLipopeptidesMice03 medical and health sciences0302 clinical medicineCandida albicansAnimalsLectins C-TypeProgenitor cellCandida albicansInnate immune systemMacrophage Colony-Stimulating FactorMacrophagesZymosanCell DifferentiationHematopoietic Stem Cellsbiology.organism_classificationToll-Like Receptor 2Cell biologyMice Inbred C57BLToll-Like Receptor 4TLR2030104 developmental biologyInfectious DiseasesTLR4Female030215 immunologyMicrobes and Infection
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Neuroendocrine Modulation of IL-27 in Macrophages

2017

Abstract Heterodimeric IL-27 (p28/EBV-induced gene 3) is an important member of the IL-6/IL-12 cytokine family. IL-27 is predominantly synthesized by mononuclear phagocytes and exerts immunoregulatory functional activities on lymphocytic and nonlymphocytic cells during infection, autoimmunity or neoplasms. There is a great body of evidence on the bidirectional interplay between the autonomic nervous system and immune responses during inflammatory disorders, but so far IL-27 has not been defined as a part of these multifaceted neuroendocrine networks. In this study, we describe the role of catecholamines (as mediators of the sympathetic nervous system) related to IL-27 production in primary …

Lipopolysaccharides0301 basic medicinemedicine.medical_specialtySympathetic nervous systemSympathetic Nervous SystemEpinephrinemedicine.medical_treatmentImmunologyInflammationMiceNorepinephrine03 medical and health sciences0302 clinical medicineFormoterol FumarateInternal medicineThiadiazolesmedicineAnimalsImmunology and AllergyAlbuterolCells CulturedAnthracenesInflammationSulfonamidesbiologyInterleukinsMacrophagesZymosanTLR7Macrophage ActivationShock SepticInterleukin-10Receptors AdrenergicToll-Like Receptor 3Mice Inbred C57BLTLR2Interleukin 10Poly I-C030104 developmental biologyCytokineEndocrinologymedicine.anatomical_structureIntegrin alpha Mbiology.proteinTLR4medicine.symptomSignal Transduction030215 immunologyThe Journal of Immunology
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Interaction of TLR2 and TLR4 ligands with the N-terminal domain of Gp96 amplifies innate and adaptive immune responses.

2006

Activation of dendritic cells by ligands for Toll-like receptors (TLR) is a crucial event in the initiation of innate and adaptive immune responses. Several classes of TLR ligands have been identified that interact with distinct members of the TLR-family. TLR4 ligands include lipopolysaccharide derived from different Gram-negative bacteria and viral proteins. Recent reports have demonstrated the TLR-mediated activation of dendritic cells by heat shock proteins (HSPs). However, doubts were raised as to what extent this effect was due to lipopolysaccharide contaminations of the HSP preparations. We re-examined this phenomenon using Gp96 or its N-terminal domain, nominally endotoxin-free (0.5 …

LipopolysaccharidesLipopolysaccharideBiologyCD8-Positive T-LymphocytesBiochemistrychemistry.chemical_compoundMiceImmune systemDogsHeat shock proteinAnimalsHumansReceptorMolecular BiologyInflammationMice Inbred BALB CInnate immune systemMembrane GlycoproteinsCCL18Cell BiologyToll-Like Receptor 2Cell biologyEndotoxinsMice Inbred C57BLToll-Like Receptor 4TLR2BiochemistrychemistryTLR4The Journal of biological chemistry
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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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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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A Pilot Study on Prostate Cancer Risk and Pro-Inflammatory Genotypes: Pathophysiology and Therapeutic Implications

2010

Host genetic factors are crucial risk determinants for many human cancers. In this framework, an interesting model is represented by prostate cancer (PC), which is featured by a complex pathophysiology with a strong genetic component. Multiple genes seem to influence PC risk and several single nucleotide polymorphisms (SNPs) of candidate genes modifying PC susceptibility have been identified. It is noteworthy the potential association of common SNPs in pro-inflammatory genes with PC risk, since chronic inflammation is assumed to play a key role in prostate carcinogenesis. With the aim to identify candidate genes as an experimental basis to develop new strategies for both prevention and trea…

MaleCandidate geneGenotypePilot ProjectsSingle-nucleotide polymorphismBioinformaticsPolymorphism Single NucleotideProstate cancerRisk FactorsDrug DiscoveryGenotypemedicineHumansSNPSettore MED/05 - Patologia ClinicaGeneAgedAged 80 and overInflammationPharmacologySettore MED/04 - Patologia Generalebusiness.industryProstatic NeoplasmsCancerMiddle AgedProstate cancer (PC) inflammation genetics TLR4 TLR2 PTGS2 5-LO SNP.medicine.diseaseImmunologyTLR4Inflammation Mediatorsbusiness
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Synergistic effect between amoxicillin and TLR ligands on dendritic cells from amoxicillin-delayed allergic patients.

2013

Journal Article; Amoxicillin, a low-molecular-weight compound, is able to interact with dendritic cells inducing semi-maturation in vitro. Specific antigens and TLR ligands can synergistically interact with dendritic cells (DC), leading to complete maturation and more efficient T-cell stimulation. The aim of the study was to evaluate the synergistic effect of amoxicillin and the TLR2, 4 and 7/8 agonists (PAM, LPS and R848, respectively) in TLR expression, DC maturation and specific T-cell response in patients with delayed-type hypersensitivity (DTH) reactions to amoxicillin. Monocyte-derived DC from 15 patients with DTH to amoxicillin and 15 controls were cultured with amoxicillin in the pr…

MaleCélulas dendríticasmedicine.medical_treatmentLymphocyte proliferationPharmacology:Chemicals and Drugs::Chemical Actions and Uses::Specialty Uses of Chemicals::Laboratory Chemicals::Ligands [Medical Subject Headings]Monocytes:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]:Phenomena and Processes::Physiological Phenomena::Pharmacological Phenomena::Pharmacological Processes::Drug Interactions::Drug Synergism [Medical Subject Headings]Cells CulturedAmoxicilinaMultidisciplinarymedicine.diagnostic_testChemistryQRLinfocitosImidazolesCitocinasMiddle AgedHumanosCytokineMedicineCytokinesFemaleDrug EruptionsResearch Article:Diseases::Skin and Connective Tissue Diseases::Skin Diseases::Exanthema [Medical Subject Headings]AdultSinergismo medicamentosoScienceFlow cytometryHipersensibilidad retardada:Chemicals and Drugs::Organic Chemicals::Amides::Lactams::beta-Lactams::Penicillins::Penicillin G::Ampicillin::Amoxicillin [Medical Subject Headings]Immune systemAntigen:Diseases::Immune System Diseases::Hypersensitivity::Hypersensitivity Delayed [Medical Subject Headings]ExantemamedicineHypersensitivity:Anatomy::Cells::Blood Cells::Leukocytes::Leukocytes Mononuclear::Lymphocytes [Medical Subject Headings]HumansLigandos:Chemicals and Drugs::Amino Acids Peptides and Proteins::Peptides::Intercellular Signaling Peptides and Proteins::Cytokines [Medical Subject Headings]:Anatomy::Cells::Antigen-Presenting Cells::Dendritic Cells [Medical Subject Headings]TLR9AmoxicillinTLR7Dendritic CellsToll-Like Receptor 2TLR2ImmunologyPloS one
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Cancer cells induce immune escape via glycocalyx changes controlled by the telomeric protein TRF2

2019

International audience; Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells with strong immunosuppressive activity that promote tumor growth. In this study, we describe a mechanism by which cancer cells control MDSCs in human cancers by upregulating TRF2, a protein required for telomere stability. Specifically, we showed that the TRF2 upregulation in cancer cells has extratelomeric roles in activating the expression of a network of genes involved in the biosynthesis of heparan sulfate proteoglycan, leading to profound changes in glycocalyx length and stiffness, as revealed by atomic force microscopy. This TRF2-dependent regulation facilitated the recruitment of MDSCs, their …

MaleHSPG;immunosurveillance;MDSC;NK cells;TRF2Mice NudeBiologyGlycocalyxGeneral Biochemistry Genetics and Molecular BiologyMetastasisGlycocalyx03 medical and health sciencesMice0302 clinical medicineDownregulation and upregulationNeoplasmsmedicineAnimalsHumansTelomeric Repeat Binding Protein 2STAT3Molecular BiologyCells Cultured030304 developmental biology0303 health sciencesGeneral Immunology and MicrobiologyGeneral NeuroscienceMyeloid-Derived Suppressor CellsArticlesTelomeremedicine.disease3. Good healthImmunosurveillanceGene Expression Regulation NeoplasticMice Inbred C57BLTLR2HEK293 CellsTumor progressionCancer cellCancer researchbiology.proteinNIH 3T3 Cells[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleTumor Escape030217 neurology & neurosurgery
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CANDIDA ALBICANS INDUCES SELECTIVE DEVELOPMENT OF MACROPHAGES AND MONOCYTE DERIVED DENDRITIC CELLS BY A TLR2 DEPENDENT SIGNALLING

2011

As TLRs are expressed by haematopoietic stem and progenitor cells (HSPCs), these receptors may play a role in haematopoiesis in response to pathogens during infection. We have previously demonstrated that in in vitro defined conditions inactivated yeasts and hyphae of Candida albicans induce HSPCs proliferation and differentiation towards the myeloid lineage by a TLR2/MyD88 dependent pathway. In this work, we showed that C. albicans invasive infection with a low virulence strain results in a rapid expansion of HSPCs (identified as LKS cells: Lin(-) c-Kit(+) Sca-1(+) IL-7R alpha(-)), that reach the maximum at day 3 post-infection. This in vivo expansion of LKS cells in TLR2(-/-) mice was del…

MaleImmune CellsCellular differentiationImmunologylcsh:MedicineMycologyMicrobiologyMonocytesMiceCandida albicansAnimalsLymphopoiesisProgenitor celllcsh:ScienceCandida albicansBiologyImmune ResponseCells CulturedMice KnockoutMultidisciplinarybiologyMacrophageslcsh:RFungal DiseasesCandidiasisCell DifferentiationHematologyDendritic CellsFlow Cytometrybiology.organism_classificationToll-Like Receptor 2Corpus albicansHematopoiesisCell biologyHost-Pathogen InteractionToll-Like Receptor 4HaematopoiesisTLR2Infectious DiseasesMyeloid Differentiation Factor 88Medicinelcsh:QFemaleStem cellInfectious Disease ModelingResearch ArticleSignal Transduction
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Mild-stretch mechanical ventilation upregulates toll-like receptor 2 and sensitizes the lung to bacterial lipopeptide.

2011

Introduction Mechanical ventilation (MV) could prime the lung toward an inflammatory response if exposed to another insult such as bacterial invasion. The underlying mechanisms are not so far clear. Toll-like receptors (TLRs) allow the host to recognize selectively bacterial pathogens and in turn to trigger an immune response. We therefore hypothesized that MV modulates TLR2 expression and in turn modifies responsiveness to agonists such as bacterial lipopeptide (BLP). Method Both in vitro and in vivo experiments were conducted. First, TLR2 expression and protein were measured in the A549 pulmonary epithelial cell line submitted to 8-hour cyclic stretch (20% elongation; 20/minute rate). Aft…

MaleInterleukin-6/metabolismCell Culture TechniquesRespiration Artificial/methodsBiologyLung injuryCritical Care and Intensive Care MedicineReal-Time Polymerase Chain Reaction03 medical and health scienceschemistry.chemical_compoundLipopeptidesToll-Like Receptor 2/analysis/genetics/metabolism0302 clinical medicineImmune systemLipopeptides/metabolismDownregulation and upregulationAnimalsReceptorLung030304 developmental biologyddc:616A549 cell0303 health sciencesToll-like receptorEpithelial Cells/metabolism/microbiologyddc:617BacteriaInterleukin-6ResearchInterleukin-8Lipopeptide030208 emergency & critical care medicineEpithelial CellsSequence Analysis DNArespiratory systemFlow CytometryRespiration ArtificialLung/immunology/metabolismToll-Like Receptor 23. Good healthCell biologyUp-RegulationTLR2chemistryInterleukin-8/metabolismBacteria/metabolismImmunologyRabbitsCritical care (London, England)
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