Search results for "TLR"

showing 10 items of 207 documents

Mast cells as rapid innate sensors of cytomegalovirus by TLR3/TRIF signaling-dependent and -independent mechanisms

2014

The succinct metaphor, ‘the immune system's loaded gun', has been used to describe the role of mast cells (MCs) due to their storage of a wide range of potent pro-inflammatory and antimicrobial mediators in secretory granules that can be released almost instantly on demand to fight invaders. Located at host–environment boundaries and equipped with an arsenal of pattern recognition receptors, MCs are destined to be rapid innate sensors of pathogens penetrating endothelial and epithelial surfaces. Although the importance of MCs in antimicrobial and antiparasitic defense has long been appreciated, their role in raising the alarm against viral infections has been noted only recently. Work on cy…

MaleChemokineImmunologyCytomegalovirusBiologyCD8-Positive T-LymphocytesCCL5MiceImmune systemImmunology and AllergyCytotoxic T cellAnimalsMast CellsMice KnockoutIntegrasesMacrophagesDegranulationPattern recognition receptorhumanitiesToll-Like Receptor 3Killer Cells NaturalMice Inbred C57BLAdaptor Proteins Vesicular TransportInfectious DiseasesTRIFImmunologyTLR3Cytomegalovirus Infectionsbiology.proteinFemaleResearch Article
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TLR4 upregulation underpins airway neutrophilia in smokers with chronic obstructive pulmonary disease and acute respiratory failure

2010

Activation of Toll-like receptors (TLR) seems to be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Upon TLR activation the release of defensins, including human beta defensin 2 (HBD-2), may occur. In this study, we explored the innate responses in patients with respiratory failure, with and without COPD, requiring intubation and mechanical ventilation. Mini-bronchoalveolar lavage (mini-BAL) samples were collected from nonsmoker subjects without COPD (n = 10), smokers without COPD (n = 6), and smokers with COPD (n = 15). TLR4, TLR2, and HBD-2 expression was evaluated by immunocytochemistry; interleukin (IL)-8, IP-10, and HBD-2 concentrations were evaluated by e…

MaleChemokinebeta-DefensinsLeukocytosisNeutrophilsLymphocyteImmunologySettore MED/41 - AnestesiologiaApoptosisPathogenesisPulmonary Disease Chronic ObstructivemedicineHumansImmunology and AllergyAgedAged 80 and overCOPDTUNEL assaybiologybusiness.industryChemotaxisInterleukin-8SmokingAcute Lung Injury COPD TLR4InterleukinGeneral Medicinemedicine.diseaseToll-Like Receptor 2Neutrophiliarespiratory tract diseasesToll-Like Receptor 4medicine.anatomical_structureTerminal deoxynucleotidyl transferaseAcute DiseaseImmunologybiology.proteinFemalemedicine.symptomRespiratory InsufficiencybusinessBronchoalveolar Lavage FluidHuman Immunology
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Toll-like receptor 5 deficiency exacerbates cardiac injury and inflammation induced by myocardial ischaemia-reperfusion in the mouse

2015

Myocardial ischaemia-reperfusion (MIR) triggers a sterile inflammatory response important for myocardial healing, but which may also contribute to adverse ventricular remodelling. Such inflammation is initiated by molecular danger signals released by damaged myocardium, which induce innate immune responses by activating toll-like receptors (TLRs). Detrimental roles have been recently reported for TLR2, TLR3 and TLR4. The role of other TLRs is unknown. We therefore evaluated the role of TLR5, expressed at high level in the heart, in the development of myocardial damage and inflammation acutely triggered by MIR. TLR5−/− and wild-type (WT) mice were exposed to MIR (30 min ischaemia, 2 h reperf…

MaleChemokinemedicine.medical_specialtyGenotypep38 mitogen-activated protein kinasesMyocardial InfarctionMyocardial Reperfusion InjuryInflammation030204 cardiovascular system & hematologyBiologyp38 Mitogen-Activated Protein KinasesVentricular Function LeftProinflammatory cytokineVentricular Dysfunction Left03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineAnimalsPhosphorylationProtein kinase B030304 developmental biologyInflammationMice Knockout0303 health sciencesToll-like receptorMyocardiumGeneral MedicineImmunity Innate3. Good healthMice Inbred C57BLDisease Models AnimalOxidative StressToll-Like Receptor 5CXCL2PhenotypeEndocrinologybiology.proteinTLR4Inflammation Mediatorsmedicine.symptomProto-Oncogene Proteins c-aktClinical Science
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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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Enhanced glomerular Toll-like receptor 4 expression and signaling in patients with type 2 diabetic nephropathy and microalbuminuria

2014

Toll-like receptor 4 (TLR4), a component of the innate immune system, is recognized to promote tubulointerstitial inflammation in overt diabetic nephropathy (DN). However, there is no information on immune activation in resident renal cells at an early stage of human DN. In order to investigate this, we studied TLR4 gene and protein expression and TLR4 downward signaling in kidney biopsies of 12 patients with type 2 diabetes and microalbuminuria, and compared them with 11 patients with overt DN, 10 with minimal change disease (MCD), and control kidneys from 13 patients undergoing surgery for a small renal mass. Both in microalbuminuria and in overt DN, TLR4 mRNA and protein were overexpress…

MaleKidney GlomerulusDiabetic nephropathyurologic and male genital diseasesDiabetic nephropathynefropatiadiabeticaDiabetic NephropathiesMinimal change diseaseChemokine CCL5KidneyMiddle AgedUp-RegulationKidney Tubulesmedicine.anatomical_structureNephrologyDisease ProgressionFemaleHumanSignal Transductionmedicine.medical_specialtyReceptors CCR5Receptors CCR2NephrosisAntigens Differentiation MyelomonocyticFollow-Up StudieNephropathyToll-like receptorAntigens CDDiabetes mellitusInternal medicinemedicineAlbuminuriaHumansRNA MessengerInflammationInterleukin-6Tumor Necrosis Factor-alphabusiness.industryNephrosis LipoidKidney TubuleTranscription Factor RelABiomarkermedicine.diseaseImmunity InnateToll-Like Receptor 4EndocrinologyDiabetes Mellitus Type 2Diabetic NephropathieTLR4MicroalbuminuriaKidney GlomerulubusinessBiomarkersMicroalbuminuriaFollow-Up StudiesKidney International
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Autoimmune skin inflammation is dependent on plasmacytoid dendritic cell activation by nucleic acids via TLR7 and TLR9

2010

Lupus-prone mice develop a chronic inflammatory response to cutaneous injury that depends on the production of type I interferon, TLR7, and TLR9.

MaleMice 129 StrainImmunologyGene ExpressionInflammationchemical and pharmacologic phenomenaMice Inbred StrainsReceptor Interferon alpha-betaBiologySkin DiseasesArticleProinflammatory cytokinePathogenesisTLR9MiceAutoimmune skin inflammationimmune system diseasesNucleic AcidsmedicineImmunology and AllergyAnimalsLupus Erythematosus SystemicReceptorskin and connective tissue diseasesTLR7SkinAutoimmune skin inflammation; TLR7; TLR9; plasmacytoid dendritic cells.Mice KnockoutPlasmacytoid dendritic cell activationLupus erythematosusReverse Transcriptase Polymerase Chain ReactionTLR9virus diseaseshemic and immune systemsTLR7DNADendritic Cellsmedicine.diseaseFlow CytometryMice Inbred C57BLplasmacytoid dendritic cells.Toll-Like Receptor 7Toll-Like Receptor 9ImmunologyMyeloid Differentiation Factor 88CytokinesFemalemedicine.symptomThe Journal of Experimental Medicine
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MyD88 is dispensable for resistance toParacoccidioides brasiliensisin a murine model of blood-borne disseminated infection

2008

We have studied the role of MyD88, an adaptor protein of Toll-like receptors (TLRs), in murine defenses against Paracoccidioides brasiliensis in a model of blood-borne disseminated infection. Wild-type (WT) and MyD88-deficient mice infected intravenously with P. brasiliensis yeast cells showed an equivalent fungal burden, as well as similar levels of proinflammatory IL-1beta, IL-6, IL-12p70, tumor necrosis factor (TNF)-alpha and MIP-2, T-helper type 1 (Th1) (IFN-gamma) and Th2 cytokines (IL-4) in tissue homogenates. In vitro production of TNF-alpha, IFN-gamma and IL-12p70, by antigen-stimulated splenocytes from infected animals, was also similar in both types of mice; this production of Th1…

MaleMicrobiology (medical)medicine.medical_treatmentImmunologyNerve Tissue ProteinsMicrobiologyParacoccidioidesMicrobiologyProinflammatory cytokineMicePeritoneal cavitymedicineAnimalsHumansImmunology and AllergyLectins C-TypeMice KnockoutParacoccidioides brasiliensisbiologyMembrane ProteinsParacoccidioidesGeneral MedicineTh1 Cellsbiology.organism_classificationToll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4Disease Models AnimalTLR2Infectious Diseasesmedicine.anatomical_structureCytokineMyeloid Differentiation Factor 88Macrophages PeritonealTLR4CytokinesTumor necrosis factor alphaParacoccidioidomycosisFungemiaFEMS Immunology & Medical Microbiology
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