Search results for "TLR"

showing 10 items of 207 documents

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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Toll-like receptor 4 defective mice carrying point or null mutations do not show increased susceptibility toCandida albicansin a model of hematogenou…

2006

We have studied the role of TLR4 in murine defenses against Candida albicans in two TLR4-defective mouse strains: C3H/HeJ mice which have defective TLR4 signaling, and TLR4-/- knockout mice. Both TLR4-defective mice strains experimentally infected with virulent C. albicans cells showed no significant difference in survival as compared with their respective controls. Recruitment of neutrophils to the peritoneal cavity of i.p. infected mice was not affected in TLR4-/-animals, but significantly enhanced in C3H/HeJ mice, compared with their control mice. In vitro production of TNF-alpha by macrophages from both types of TLR4-defective mice, in response to yeasts and hyphae of C. albicans, was n…

MaleNeutrophilsBiologyMicrobiologyInterferon-gammaMicePeritoneal cavityCandida albicansSplenocytemedicineAnimalsPoint MutationGenetic Predisposition to DiseaseCandida albicansMice KnockoutMice Inbred C3HToll-like receptorTumor Necrosis Factor-alphaCandidiasisGeneral MedicineTh1 CellsFlow Cytometrybiology.organism_classificationInterleukin-12Corpus albicansMice Inbred C57BLToll-Like Receptor 4Infectious Diseasesmedicine.anatomical_structureKnockout mouseMacrophages PeritonealTLR4Femalelipids (amino acids peptides and proteins)Tumor necrosis factor alphaMedical Mycology
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Polymorphisms of an innate immune gene, toll-like receptor 4, and aggressive prostate cancer risk: a systematic review and meta-analysis.

2014

Background: Toll-like receptor 4 (TLR4) is one of the best known TLR members expressed on the surface of several leukocytes and tissue cells and has a key function in detecting pathogen and danger-associated molecular patterns. The role of TLR4 in the pathophysiology of several age-related diseases is also well recognized, such as prostate cancer (PCa). TLR4 polymorphisms have been related to PCa risk, but the relationship between TLR4 genotypes and aggressive PCa risk has not been evaluated by any systematic reviews. Methods: We performed a systematic review and meta-analysis of candidate-gene and genome-wide association studies analyzing this relationship and included only white populatio…

MaleProstate cancer polymorphisms of TLR4 aggressive prostate cancer risk meta-analysisSystematic Reviewslcsh:MedicineGenome-wide association studySingle-nucleotide polymorphismBiologyResearch and Analysis MethodsBioinformaticsPolymorphism Single NucleotideProstate cancerGenotypeGeneticsCancer GeneticsmedicineHumansSettore MED/05 - Patologia ClinicaGenetic Predisposition to DiseaseStatistical Methodslcsh:ScienceGenotypingGenetic associationEvolutionary BiologyMultidisciplinarylcsh:RProstatic NeoplasmsBiology and Life SciencesResearch Assessmentmedicine.diseaseImmunity InnateToll-Like Receptor 4Systematic reviewMeta-analysisPhysical SciencesGenetic Polymorphismlcsh:QPopulation GeneticsMathematicsStatistics (Mathematics)Genome-Wide Association StudyResearch ArticleMeta-AnalysisPLoS ONE
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Interruption of Macrophage-Derived IL-27(p28) Production by IL-10 during Sepsis Requires STAT3 but Not SOCS3

2014

Abstract Severe sepsis and septic shock are leading causes of morbidity and mortality worldwide. Infection-associated inflammation promotes the development and progression of adverse outcomes in sepsis. The effects of heterodimeric IL-27 (p28/EBI3) have been implicated in the natural course of sepsis, whereas the molecular mechanisms underlying the regulation of gene expression and release of IL-27 in sepsis are poorly understood. We studied the events regulating the p28 subunit of IL-27 in endotoxic shock and polymicrobial sepsis following cecal ligation and puncture. Neutralizing Abs to IL-27(p28) improved survival rates, restricted cytokine release, and reduced bacterial burden in C57BL/…

MaleSTAT3 Transcription Factormedicine.medical_treatmentImmunologySuppressor of Cytokine Signaling ProteinsInflammationSpleenBiologyArticleSepsisMiceSepsismedicineAnimalsHumansImmunology and AllergyReceptors CytokineAntibodies BlockingCecumCells CulturedMice KnockoutSeptic shockInterleukinsMacrophagesReceptors Interleukinmedicine.diseaseBacterial LoadInterleukin-10Mice Inbred C57BLToll-Like Receptor 4Adaptor Proteins Vesicular TransportDisease Models AnimalOxidative StressInterleukin 10Cytokinemedicine.anatomical_structureIntegrin alpha MSuppressor of Cytokine Signaling 3 ProteinMyeloid Differentiation Factor 88ImmunologyTLR4biology.proteinmedicine.symptomJournal of Immunology
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TLR4 response mediates ethanol-induced neurodevelopment alterations in a model of fetal alcohol spectrum disorders

2017

Background Inflammation during brain development participates in the pathogenesis of early brain injury and cognitive dysfunctions. Prenatal ethanol exposure affects the developing brain and causes neural impairment, cognitive and behavioral effects, collectively known as fetal alcohol spectrum disorders (FASD). Our previous studies demonstrate that ethanol activates the innate immune response and TLR4 receptor and causes neuroinflammation, brain damage, and cognitive defects in the developmental brain stage of adolescents. We hypothesize that by activating the TLR4 response, maternal alcohol consumption during pregnancy triggers the release of cytokines and chemokines in both the maternal …

MaleSerum0301 basic medicineChemokineDevelopmental Disabilitiesmedicine.medical_treatmentlcsh:RC346-429MiceMyelin0302 clinical medicineNeuroinflammationPregnancyTLR4Maternal BehaviorFetal alcohol spectrum disordersMice KnockoutMicrogliabiologyGeneral NeuroscienceAge FactorsBrainCerebral cortexBehavior impairmentsmedicine.anatomical_structureCytokineNeurologyPrenatal Exposure Delayed EffectsCytokinesFemalemedicine.symptomMyelin ProteinsAmniotic fluidmedicine.medical_specialtyOffspringImmunologyNerve Tissue ProteinsBrain damage03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicineAvoidance LearningmedicineAnimalsMaze Learninglcsh:Neurology. Diseases of the nervous systemNeuroinflammationEthanolbusiness.industryResearchBody WeightCentral Nervous System DepressantsMice Inbred C57BLToll-Like Receptor 4Disease Models AnimalMicroscopy Electron030104 developmental biologyEndocrinologyAnimals NewbornPrenatal ethanol exposureImmunologybiology.proteinTLR4business030217 neurology & neurosurgeryJournal of Neuroinflammation
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RNA recognition by human TLR8 can lead to autoimmune inflammation

2013

High expression level of human TLR8 in mice results in spontaneous, multiorgan inflammation attributable in part to increased DC activation.

MaleT cellT-LymphocytesImmunologyArthritisInflammationMice TransgenicAutoimmunityTRL8AUTOIMMUNE INFLAMMATIONBiologymedicine.disease_causeArticleAutoimmunityProinflammatory cytokineMiceTRL8; AUTOIMMUNE INFLAMMATIONhemic and lymphatic diseasesmedicineImmunology and AllergyAnimalsHumansTransgenesChildRandomized Controlled Trials as TopicInflammationGene Expression ProfilingTLR7TLR8medicine.diseaseArthritis Experimentaldigestive system diseasesArthritis JuvenileMice Inbred C57BLmedicine.anatomical_structureToll-Like Receptor 7Toll-Like Receptor 8ImmunologyRNAFemaleCollagenSignal transductionmedicine.symptomSignal TransductionThe Journal of Experimental Medicine
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Wheat Consumption Aggravates Colitis in Mice via Amylase Trypsin Inhibitor–mediated Dysbiosis

2020

Background & Aims Wheat has become the world's major staple and its consumption correlates with prevalence of noncommunicable disorders such as inflammatory bowel diseases. Amylase trypsin inhibitors (ATIs), a component of wheat, activate the intestine's innate immune response via toll-like receptor 4 (TLR4). We investigated the effects of wheat and ATIs on severity of colitis and fecal microbiota in mice. Methods C57BL/6 wild-type and Tlr4–/– mice were fed wheat- or ATI-containing diets or a wheat-free (control) diet and then given dextran sodium sulfate to induce colitis; we also studied Il10–/– mice, which develop spontaneous colitis. Changes in fecal bacteria were assessed by taxa-speci…

MaleTrypsin inhibitorPlant Proteins DietarySeverity of Illness IndexInflammatory bowel diseaseMicrobiologyFecesMicemedicineAnimalsHumansAmylaseColitisTriticumFecesMice KnockoutHepatologybiologyDextran SulfateGastroenterologyfood and beveragesFecal Microbiota TransplantationColitisInflammatory Bowel Diseasesmedicine.diseaseAnimal FeedImmunity InnateGastrointestinal MicrobiomeToll-Like Receptor 4TransplantationDisease Models Animalbiology.proteinTLR4DysbiosisTrypsin InhibitorsDysbiosisSignal TransductionGastroenterology
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TLR7 and TLR8 ligands and antiphospholipid antibodies show synergistic effects on the induction of IL-1beta and caspase-1 in monocytes and dendritic …

2009

TLRs represent the first line of defense against invading pathogens in the innate immune system. Certain cytokines are important mediators and essentially necessary to assure an appropriately regulated immune response. Recent data gave initial evidence that IL-1beta is one of the most relevant members of these regulating cytokines. We investigated the induction of IL-1beta production in monocytes and pDCs stimulated with ligands for TLR7 and TLR8 and with antiphospholipid antibodies (aPL). Using human monocytes and pDCs for stimulation with specific TLR7 and TLR8 ligands such as resiquimod (R848) and single stranded RNA (RNA42) as well as with a human monoclonal aPL HL5B resulted in a speci…

Malemedicine.drug_classImmunologyInterleukin-1betaCaspase 1Enzyme-Linked Immunosorbent AssayCell SeparationBiologyRegulatory Sequences Nucleic AcidMonoclonal antibodyLigandsMonocytesProinflammatory cytokinechemistry.chemical_compoundImmune systemmedicineImmunology and AllergyHumansInnate immune systemCaspase 1ImidazolesHematologyTLR7Dendritic CellsTLR8Oligonucleotides AntisenseAntiphospholipid SyndromeFlow CytometrychemistryToll-Like Receptor 7Toll-Like Receptor 8Enzyme InductionImmunologyAntibodies AntiphospholipidRNAFemaleResiquimodImmunobiology
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TLR4 polymorphisms and ageing: implications for the pathophysiology of age-related diseases.

2009

Innate immunity provides a first line of host defense against infection by recognizing and killing microbes while simultaneously activating an instructive immune response. Toll-like receptors (TLRs) are principal mediators of rapid microbial recognition and function mainly by detection of pathogen-associated molecular patterns that do not exist in the host. Recognition of their ligands leads to a series of signaling events resulting in acute host responses, involved in killing pathogens. Discussion We describe the involvement of TLR4 polymorphisms in ageing, and in particular in age-related diseases, suggesting the crucial role of molecules of innate immunity in pathophysiology of these dis…

Malemedicine.medical_specialtyAgingImmunologyLongevitySNPBiologyPolymorphism Single NucleotideatherosclerosiImmune systemMedical microbiologyAlzheimer DiseasemedicinecancerImmunology and AllergyHumansGenetic Predisposition to DiseaseTLR4Receptorinnate immunityAllelesSettore MED/04 - Patologia GeneraleInnate immune systemHost (biology)Prostatic Neoplasmsmedicine.diseaseImmunity InnateToll-Like Receptor 4AgeingCardiovascular DiseasesImmunologyTLR4FemaleAlzheimer's diseaseAlzheimer’s diseaseFunction (biology)Journal of clinical 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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