Search results for "Toll-Like Receptor 2"

showing 10 items of 46 documents

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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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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Dectin-1 Stimulation of Hematopoietic Stem and Progenitor Cells Occurs In Vivo and Promotes Differentiation Toward Trained Macrophages via an Indirec…

2020

Invasive candidiasis is an increasingly frequent cause of serious and often fatal infections. Understanding host defense is essential to design novel therapeutic strategies to boost immune protection against Candida albicans. In this article, we delve into two new concepts that have arisen over the last years: (i) the delivery of myelopoiesis-inducing signals by microbial components directly sensed by hematopoietic stem and progenitor cells (HSPCs) and (ii) the concept of “trained innate immunity” that may also apply to HSPCs. We demonstrate that dectin-1 ligation in vivo activates HSPCs and induces their differentiation to trained macrophages by a cell-autonomous indirect mechanism. This p…

MaleMyeloidbeta-Glucanshematopoietic stem and progenitor cellstlr2BiologyMicrobiologyHost-Microbe Biology03 medical and health sciencesMicetrained immunity0302 clinical medicineImmune systemVirologymedicineAnimalsLectins C-TypeProgenitor cell030304 developmental biologyMice Knockout0303 health sciencesInnate immune systemStem CellsCandidiasisCell DifferentiationHematopoietic Stem CellsImmunity InnateToll-Like Receptor 2QR1-502Cell biologymacrophagesTransplantationMice Inbred C57BLTLR2Haematopoiesismedicine.anatomical_structureMyeloid Differentiation Factor 88Femalecandida albicansBone marrowdectin-1030215 immunologyResearch ArticleSignal TransductionmBio
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Susceptibility to infection with Borrelia afzelii and TLR2 polymorphism in a wild reservoir host

2019

AbstractThe study of polymorphic immune genes in host populations is critical for understanding genetic variation in susceptibility to pathogens. Controlled infection experiments are necessary to separate variation in the probability of exposure from genetic variation in susceptibility to infection, but such experiments are rare for wild vertebrate reservoir hosts and their zoonotic pathogens. The bank vole (Myodes glareolus) is an important reservoir host of Borrelia afzelii, a tick-borne spirochete that causes Lyme disease. Bank vole populations are polymorphic for Toll-like receptor 2 (TLR2), an innate immune receptor that recognizes bacterial lipoproteins. To test whether the TLR2 polym…

MaleNymph0301 basic medicinemetsämyyrälcsh:MedicineTickBorrelia afzeliimedicine.disease_causeinfektiotgenotyyppiArticle03 medical and health sciencesTicks0302 clinical medicineLyme diseaseBorrelia burgdorferi GroupPolymorphism (computer science)GenotypeGenetic variationparasitic diseasesisäntäeläimetImmunogeneticsmedicineAnimalsimmuniteettiGenetic Predisposition to Diseaselcsh:ScienceDisease ReservoirsGeneticsLyme DiseasePolymorphism GeneticMultidisciplinaryInnate immune systembiologyArvicolinaelcsh:REcological geneticsmedicine.diseasebiology.organism_classificationbacterial infections and mycosesToll-Like Receptor 2Borrelia-bakteeritBank vole030104 developmental biology[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyFemalelcsh:Q030217 neurology & neurosurgeryClethrionomys
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High Dimensional Immune Profiling Reveals Different Response Patterns in Active and Latent Tuberculosis Following Stimulation With Mycobacterial Glyc…

2021

Upon infection withMycobacterium tuberculosis(Mtb) the host immune response might clear the bacteria, control its growth leading to latent tuberculosis (LTB), or fail to control its growth resulting in active TB (ATB). There is however no clear understanding of the features underlying a more or less effective response. Mtb glycolipids are abundant in the bacterial cell envelope and modulate the immune response to Mtb, but the patterns of response to glycolipids are still underexplored. To identify the CD45+leukocyte activation landscape induced by Mtb glycolipids in peripheral blood of ATB and LTB, we performed a detailed assessment of the immune response of PBMCs to the Mtb glycolipids lip…

Maleactive tuberculosis (ATB)T-LymphocytesPhosphatidylinositolsCohort Studies0302 clinical medicineImmunology and AllergyMyeloid CellsProspective StudiesOriginal ResearchAged 80 and overB-Lymphocytes0303 health sciencesLatent tuberculosishyporesponsivenessMiddle Aged3. Good healthphosphatidylinositol mannoside (PIM)Killer Cells NaturalCytokineslipids (amino acids peptides and proteins)Femalelatent tuberculosis (LTB)AdultImmunologymycobacterial glycolipidschemical and pharmacologic phenomenaIn Vitro TechniquesBiologyTuberculinPeripheral blood mononuclear cellMicrobiologyProinflammatory cytokineMycobacterium tuberculosisYoung Adult03 medical and health sciencesGlycolipidImmune systemLatent TuberculosismedicineHumansTuberculosisMass cytometryAged030304 developmental biologyAntigens BacterialLipoarabinomannanlipoarabinomannan (LAM)Mycobacterium tuberculosisRC581-607bacterial infections and mycosesmedicine.diseasebiology.organism_classificationToll-Like Receptor 2Case-Control StudiesImmunologic diseases. AllergyGlycolipids030215 immunologyFrontiers in Immunology
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Toll-like receptor 2 mediates prostaglandin E2 production in murine peritoneal macrophages and splenocytes in response to Candida albicans

2004

The involvement of Toll-like receptor 2 (TLR2) and TLR4 in triggering signal transduction pathways leading to prostaglandin E(2) (PGE(2)) production in response to Candida albicans has been studied in cells from wild-type, TLR2-/- and TLR4-/- knockout mice. In vitro PGE(2) production by macrophages challenged with zymosan, yeast or hypha cells was strongly inhibited in TLR2-deficient cells, but not in TLR4-/- cells, as compared to macrophages from wild-type mice. PGE(2) production was dependent on de novo cyclooxygenase-2 (Cox2) synthesis, since unchallenged cells failed to produce PGE(2) and specific Cox2 inhibition during challenge totally blocked PGE(2) production. Similar results were o…

Malemedicine.medical_treatmentReceptors Cell SurfaceBiologyMicrobiologyDinoprostoneMicechemistry.chemical_compoundCandida albicansmedicineAnimalsProstaglandin E2Candida albicansMolecular BiologyCells CulturedMice KnockoutToll-like receptorZymosanGeneral Medicinebiology.organism_classificationMolecular biologyToll-Like Receptor 2Corpus albicansToll-Like Receptor 4TLR2chemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesImmunologyMacrophages PeritonealTLR4Femalelipids (amino acids peptides and proteins)Signal Transductionmedicine.drugProstaglandin EResearch in Microbiology
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TLR2: for or against Candida albicans?

2005

In a recent issue of Trends in Microbiology, Netea and coworkers presented their opinion that toll-like receptors (TLRs) are involved in escape from the defense mechanisms of the host [1]. In their article, the authors clearly identified three major TLR-mediated escape mechanisms that are used by microbial pathogens, such as Yersinia, Mycobacterium and Candida. Here, we wish to comment on the roll of TLR2 in Candida albicans infections. Netea's interesting hypothesis, that TLR2 expression might confer to mice an increased susceptibility to C.

Microbiology (medical)biologyHost (biology)Defence mechanismsCandidiasisYersiniabiology.organism_classificationMicrobiologyToll-Like Receptor 2MicrobiologyTLR2MiceInfectious DiseasesVirologyCandida albicansImmune ToleranceAnimalsReceptors ImmunologicCandida albicansReceptorMycobacteriumTrends in microbiology
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About the role of TLR2 and TLR4 in cytokine secretion by murine macrophages in response to Candida albicans.

2006

Dear Editor, In a recent issue of FEMS Immunology and Medical Microbiology , Blasi (2005) studied the biological role of Toll-like receptor (TLR)2 and TLR4 in the effector and secretory responses of murine macrophages to the fungal species Candida albicans . In their article, the authors conclude that the secretory response to C. albicans appears to be TLR4- but not TLR2-dependent. In our opinion this statement is misleading as the results reported do not support this conclusion and, therefore, we wish to comment on this issue. There is evidence indicating that TLR2 is the main receptor involved in triggering cytokine production by murine macrophages in response to C. albicans . Phospholipo…

Microbiology (medical)medicine.medical_treatmentImmunologyMicrobiologyMicrobiologyMiceCandida albicansmedicineImmunology and AllergyAnimalsCandida albicansbiologyEffectorMacrophagesCandidiasisGeneral Medicinebiology.organism_classificationCorpus albicansToll-Like Receptor 2Toll-Like Receptor 4TLR2Infectious DiseasesCytokineImmunologyTLR4CytokinesCytokine secretionTumor necrosis factor alphaFEMS immunology and medical microbiology
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Signalling through TLR2/MyD88 induces differentiation of murine bone marrow stem and progenitor cells to functional phagocytes in response to Candida…

2009

Summary We have previously demonstrated that inactivated yeasts and hyphae of Candida albicans induce in vitro the proliferation of murine haematopoietic stem and progenitor cells (HSPCs, sorted as LKS cells: Lin - c-Kit + Sca-1 + ) as well as their differentia- tion to lineage-positive cells, through a MyD88- dependent pathway. In this work, we have found that this process is mainly mediated by TLR2, and that expanding cells express myeloid and not lym- phoid markers. Incubation of long-term repopulat- ing HSCs (Lin - CD105 + and Sca-1 + ) with C. albicans yeasts resulted in their proliferation and up regu- lation of the common myeloid progenitors (CMPs) markers, CD34 and FcgRII/III, by a …

MyeloidCellular differentiationImmunologyCD34Bone Marrow CellsMicrobiologyMiceVirologyCandida albicansmedicineMacrophageAnimalsAntigens LyProgenitor cellCandida albicansCells CulturedPhagocytesCD11b AntigenbiologyStem CellsCell Differentiationbiology.organism_classificationFlow CytometryAntigens DifferentiationMice Mutant StrainsToll-Like Receptor 2Cell biologyHaematopoiesismedicine.anatomical_structureMyeloid Differentiation Factor 88Bone marrowSignal TransductionCellular microbiology
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EBV-Induced Gene 3 Transcription Is Induced by TLR Signaling in Primary Dendritic Cells via NF-κB Activation

2005

Abstract The EBV-induced gene 3 (EBI3) is expressed in dendritic cells (DCs) and part of the cytokine IL-27 that controls Th cell development. However, its regulated expression in DCs is poorly understood. In the present study we demonstrate that EBI3 is expressed in splenic CD8−, CD8+, and plasmacytoid DC subsets and is induced upon TLR signaling. Cloning and functional analysis of the EBI3 promoter using in vivo footprinting and mutagenesis showed that stimulation via TLR2, TLR4, and TLR9 transactivated the promoter in primary DCs via NF-κB and Ets binding sites at −90 and −73 bp upstream of the transcriptional start site, respectively. Furthermore, we observed that NF-κB p50/p65 and PU.1…

RNA Capsmedicine.medical_treatmentDNA Mutational AnalysisMolecular Sequence DataImmunologyAntigen-Presenting CellsReceptors Cell SurfaceBiologyCell LineMinor Histocompatibility AntigensJurkat CellsMiceCell Line TumorGene expressionmedicineAnimalsHumansImmunology and AllergyReceptors CytokinePromoter Regions GeneticGlycoproteinsMice KnockoutMembrane GlycoproteinsInnate immune systemBase SequenceToll-Like ReceptorsHEK 293 cellsNF-kappa BTLR9hemic and immune systemsEBI3Dendritic CellsMolecular biologyToll-Like Receptor 2Up-RegulationMice Inbred C57BLToll-Like Receptor 4Protein SubunitsTLR2CytokineGene Expression RegulationToll-Like Receptor 9NIH 3T3 CellsTLR4Protein BindingSignal TransductionThe Journal of Immunology
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