Search results for " TLR"

showing 10 items of 28 documents

1-ethyl-3-(6-methylphenanthridine-8-il) urea modulates TLR3/9 activation and induces selective pro-inflammatory cytokine expression in vitro.

2017

We have previously demonstrated the nucleic acid binding capacity of phenanthridine derivatives (PHTs). Because nucleic acids are potent inducers of innate immune response through Toll-like receptors (TLRs), and because PTHs bear a structural resemblance to commonly used synthetic ligands for TLR7/8, we hypothesized that PHTs could modulate/activate immune response. We found that compound M199 induces secretion of IL-6, IL-8 and TNFα in human PBMCs and inhibits TLR3/9 activation in different cellular systems (PBMCs, HEK293 and THP-1 cell lines).

0301 basic medicineClinical BiochemistryPharmaceutical ScienceDown-RegulationBiochemistryCell Line03 medical and health sciences0302 clinical medicineImmune systemDrug DiscoveryHumansImmunologic FactorsUreaSecretionReceptorMolecular BiologyInnate immune systemChemistryInterleukin-6Tumor Necrosis Factor-alphaOrganic ChemistryInterleukin-8Interferon-alphaTLR7Molecular biologyphenantridines ; TLR ; PBMCs ; cytokines ; immunomodulationIntercalating AgentsPhenanthridinesToll-Like Receptor 3030104 developmental biologyOligodeoxyribonucleotidesToll-Like Receptor 9TLR3Nucleic acidMolecular MedicineTumor necrosis factor alpha030215 immunologySignal TransductionBioorganicmedicinal chemistry letters
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Myeloid Cells Restrict MCMV and Drive Stress- Induced Extramedullary Hematopoiesis through STAT1

2019

Cytomegalovirus (CMV) has a high prevalence worldwide, is often fatal for immunocompromised patients, and causes bone marrow suppression. Deficiency of signal transducer and activator of transcription 1 (STAT1) results in severely impaired antiviral immunity. We have used cell- type restricted deletion of Stat1 to determine the importance of myeloid cell activity for the defense against murine CMV (MCMV). We show that myeloid STAT1 limits MCMV burden and infection- associated pathology in the spleen but does not affect ultimate clearance of infection. Unexpectedly, we found an essential role of myeloid STAT1 in the induction of extramedullary hematopoiesis (EMH). The EMH- promoting function…

0301 basic medicineMaleMuromegalovirusMyeloidIFN-II receptorReceptor Interferon alpha-betamonocytes signal transducer and activator of transcription Herpesviridae IFN-I receptor IFN-II receptor L-27 receptor TLR9 agonistmedicine.disease_causeVirus Replication0302 clinical medicineTLR9 agonistMyeloid CellsSTAT1Cells CulturedHerpesviridaeReceptors Interferonsignal transducer and activator of transcriptionvirus diseasesIL-27 receptorHerpesviridae InfectionsExtramedullary hematopoiesisKiller Cells NaturalHaematopoiesismedicine.anatomical_structureSTAT1 Transcription FactorBone marrow suppressionHematopoiesis ExtramedullaryFemalemonocytesBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.SpleenBiologyGeneral Biochemistry Genetics and Molecular BiologyHerpesviridaeArticle03 medical and health sciencesStress PhysiologicalmedicineAnimalsBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.Receptors Interleukinmedicine.diseaseMice Inbred C57BL030104 developmental biologyImmunologySTAT proteinbiology.protein030217 neurology & neurosurgeryGene DeletionSpleenIFN-I receptor
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Biomarkers for vascular ageing in aorta tissues and blood samples.

2019

Abstract Objectives Functional and quantitative alterations and senescence of circulating and expanded endothelial progenitor cells (EPC), as well as systemic and tissue modifications of angiogenetic and inflammatory molecules, were evaluated for predicting age-related vessel wall remodeling, correlating them to intima media thickness (IMT) in the common carotid artery (CCA), a biomarker of early cardiovascular disease and aortic root dilation. Populations and methods A homogenous Caucasian population was included in the study, constituted by 160 healthy subjects (80 old subjects, mean age 72 ± 6.4, range 66–83 years; and 80 younger blood donors, mean age 26.2 ± 3.4, range 21–33 years), and…

0301 basic medicineMaleVascular Endothelial Growth Factor AAgingPhysiologySystemic inflammationBiochemistryCarotid Intima-Media Thickness0302 clinical medicineEndocrinologySA-β-Gal activityp21 and p16 genesMedicineTP53Receptor Notch1AortaEndothelial Progenitor CellsAged 80 and overeducation.field_of_studyChemotaxisInflammatory cytokinesmedicine.anatomical_structurecardiovascular systemBiomarker (medicine)Femalemedicine.symptomTP53 p21 and p16 genesSenescenceAdultEndotheliumInflammatory cytokineNotch and TLR4Carotid Artery CommonPopulationProinflammatory cytokine03 medical and health sciencesYoung AdultTP53 p21 and p16 genemedicine.arteryGeneticsHumansEPC cell populationeducationMolecular BiologyEPC cell populationsAgedAortabusiness.industryEndothelium age-related impairmentCell BiologyChemokine CXCL12Toll-Like Receptor 4EPC cell populations; Endothelium age-related impairment; Inflammatory cytokines; Notch and TLR4; SA-β-Gal activity; TP53 p21 and p16 genesSettore MED/23030104 developmental biologyIntima-media thicknessbusiness030217 neurology & neurosurgeryBiomarkersExperimental gerontology
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Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

2017

Recent advances in the field of innate immunity have revealed a complex role of innate immune signaling pathways in both tissue homeostasis and disease. Among them, the Toll-like receptor 4 (TLR-4) pathways has been linked to various pathophysiological conditions, such as cardiovascular diseases (CVDs). This has been interrogated by developing multiple laboratory tools that have shown in animal models and clinical conditions, the involvement of the TLR-4 signaling pathway in the pathophysiology of different CVDs, such as atherosclerosis, ischemic heart disease, heart failure, ischemia-reperfusion injury and aorta aneurysm. Among these, aorta aneurysm, a very complex pathological condition w…

0301 basic medicinePathologymedicine.medical_specialtyAgingDisease030204 cardiovascular system & hematologyBioinformatics03 medical and health sciences0302 clinical medicineAneurysmAorta; Aorta aneurysms; TLR-4 signaling pathway; Treatments; Aging; Animals; Aorta; Cardiovascular Diseases; Homeostasis; Humans; Toll-Like Receptor 4; Signal TransductionAorta aneurysmsmedicine.arterymedicineSettore MED/05 - Patologia ClinicaAnimalsHomeostasisHumansMolecular BiologyTissue homeostasisAortaToll-like receptorAortaAorta; Aorta aneurysms; TLR-4 signaling pathway; TreatmentsInnate immune systembusiness.industryTreatmentsTLR-4 signaling pathwaySettore MED/23 - Chirurgia Cardiacamedicine.diseaseToll-Like Receptor 4030104 developmental biologyCardiovascular DiseasesHeart failurecardiovascular systemAorta aneurysmSignal transductionCardiology and Cardiovascular MedicinebusinessSignal Transduction
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Bronchial inflammation and bacterial load in stable COPD is associated with TLR4 overexpression.

2017

Toll-like receptors (TLRs) and nucleotide-binding oligomerisation domain (NOD)-like receptors (NLRs) are two major forms of innate immune sensors but their role in the immunopathology of stable chronic obstructive pulmonary disease (COPD) is incompletely studied. Our objective here was to investigate TLR and NLR signalling pathways in the bronchial mucosa in stable COPD.Using immunohistochemistry, the expression levels of TLR2, TLR4, TLR9, NOD1, NOD2, CD14, myeloid differentiation primary response gene 88 (MyD88), Toll-interleukin-1 receptor domain-containing adaptor protein (TIRAP), and the interleukin-1 receptor-associated kinases phospho-IRAK1 and IRAK4 were measured in the bronchial muc…

0301 basic medicineTIRAPMaleRespiratory SystemVital CapacityHAEMOPHILUS-INFLUENZAELUNG MICROBIOMEPathogenesisPulmonary Disease Chronic Obstructive0302 clinical medicineNOD2ImmunopathologyForced Expiratory VolumeNod1 Signaling Adaptor ProteinNOD1PhosphorylationCOPDSmoking11 Medical And Health SciencesMiddle AgedCPG-DNAbronchial inflammationAnti-Bacterial AgentsStreptococcus pneumoniaePseudomonas aeruginosaMOUSE LUNGFemaleLife Sciences & BiomedicineMoraxella catarrhalisSignal TransductionEXPRESSIONPulmonary and Respiratory MedicineCD14BronchiRespiratory MucosaReal-Time Polymerase Chain ReactionOBSTRUCTIVE PULMONARY-DISEASETLRs NLR bronchial inflammationNLRDENDRITIC CELL SUBSETS03 medical and health sciencesProtein DomainsmedicineHumansTLRsAgedTOLL-LIKE RECEPTORSCOPD TLR4InflammationScience & TechnologyBacteriabusiness.industrymedicine.diseaseHaemophilus influenzaeBacterial Loadrespiratory tract diseasesToll-Like Receptor 4TLR2030104 developmental biology030228 respiratory systemImmunologyINNATE IMMUNITYT-CELLSbusinessThe European respiratory journal
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HSP60 activity on human bronchial epithelial cells

2017

HSP60 has been implicated in chronic inflammatory disease pathogenesis, including chronic obstructive pulmonary disease (COPD), but the mechanisms by which this chaperonin would act are poorly understood. A number of studies suggest a role for extracellular HSP60, since it can be secreted from cells and bind Toll-like receptors; however, the effects of this stimulation have never been extensively studied. We investigated the effects (pro- or anti-inflammatory) of HSP60 in human bronchial epithelial cells (16-HBE) alone and in comparison with oxidative, inflammatory, or bacterial challenges. 16-HBE cells were cultured for 1–4 h in the absence or presence of HSP60, H2O2, lipopolysaccharide (…

0301 basic medicinep38αSettore BIO/17 - IstologiaLipopolysaccharidep38 mitogen-activated protein kinasesImmunologyStimulationBronchip38 Mitogen-Activated Protein KinasesERK1Cell LinePathogenesisMitochondrial Proteins03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOriginal Research ArticlesHumansImmunology and AllergyCOPDInterleukin 8Protein kinase AReceptor16-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; TLR-4; p38αPharmacologyIL-8Settore BIO/16 - Anatomia UmanaInterleukin-8JNK1NF-κB p65 subunitEpithelial CellsTLR-4Chaperonin 60MyD88Interleukin-1016-HBEToll-Like Receptor 416-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; p38α; TLR-4; Immunology and Allergy; Immunology; PharmacologyInterleukin 10030104 developmental biologychemistry030220 oncology & carcinogenesisIL-10Cancer researchCREB1NF-κB p65 subunitHSP60p38α
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Implicación de los receptores TLR4 en el daño cerebral causado por el consumo de alcohol

2012

El abuso de alcohol puede causar daño cerebral y en ciertos casos cursa con neurodegeneración, aunque los mecanismos moleculares de estos efectos se desconocen. El Sistema Nervioso Central (SNC) ha sido considerado, hasta muy recientemente, como un sistema inmunológicamente privilegiado (Galea et al., 2007). Sin embargo, estudios de los últimos años indican que el cerebro coordina y regula numerosos aspectos de la respuesta inmune innata, y que la inflamación representa un factor crítico y esencial para muchas enfermedades del SNC, como son las enfermedades neurodegenerativas (Wild et al., 2008). Igualmente, la respuesta del sistema inmune innato también desempeña un papel crucial en el dañ…

ALCOHOL; DAÑO CEREBRAL; RECEPTORES TLR4; INFLAMASOMA NLRP3UNESCO::CIENCIAS MÉDICAS ::ToxicologíaRECEPTORES TLR4:CIENCIAS DE LA VIDA::Biología celular::Cultivo celular [UNESCO]UNESCO::CIENCIAS DE LA VIDA::NeurocienciasDAÑO CEREBRALUNESCO::CIENCIAS DE LA VIDA::Biología celular::Cultivo celularALCOHOL:CIENCIAS DE LA VIDA::Neurociencias [UNESCO]INFLAMASOMA NLRP3:CIENCIAS MÉDICAS ::Patología [UNESCO]UNESCO::CIENCIAS MÉDICAS ::Patología:CIENCIAS MÉDICAS ::Toxicología [UNESCO]
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LPS-mediated production of pro/anti-inflammatory cytokines and eicosanoids in whole blood samples: Biological effects of +896A/G TLR4 polymorphism in…

2011

Toll-like receptors (TLRs) are the principal mediators of rapid microbial recognition: the lipopolysaccharide (LPS) receptor TLR4 seems to have a paradigmatic role. Single nucleotide polymorphisms (SNPs) in the TLR4 gene, such as +896A/G, known to attenuate receptor signaling, have been described. The +896A/G SNP is significantly less frequent in patients with myocardial infarction, Alzheimer's disease or prostate cancer, whereas it is overrepresented in centenarians. To clarify and confirm the biological effects of +896A/G SNP and its role in the pathophysiology of age-related diseases and longevity, we assessed the levels of IL-6, TNF-α, IL-10 and eicosanoids (LTB4 and PGE2) in LPS-stimul…

AdultLipopolysaccharidesMaleAgingAgeing Cytokines Eicosanoids Genetics Inflammation Longevity TLR4PopulationInflammationSingle-nucleotide polymorphismBiologyLeukotriene B4Polymorphism Single NucleotideDinoprostonemedicineHumansSNPeducationReceptorSettore MED/04 - Patologia Generaleeducation.field_of_studyMiddle AgedToll-Like Receptor 4ItalyEicosanoidImmunologyTLR4CytokinesFemalelipids (amino acids peptides and proteins)medicine.symptomDevelopmental BiologyEicosanoid ProductionMechanisms of Ageing and Development
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Distinct single-component adjuvants steer human DC-mediated T-cell polarization via Toll-like receptor signaling toward a potent antiviral immune res…

2021

Significance Vaccines profit from the addition of adjuvants to better and more specifically initiate, amplify, and shape immune responses. Although the number of adjuvant candidates has steadily increased, peaking in the current SARS-CoV-2 pandemic, little is known about their inherent mode of action. Using human blood immune cells, we established a multilayer method to systematically assess the adjuvants’ effects on innate and adaptive immune cells. By employing a multiplex analysis with cells from 30 different donors, we determined important patterns of adjuvant function. Moreover, we demonstrate correlates of an antiviral immune response using a Toll-like receptor 7/8 ligand adjuvant and…

AdultMaleAdolescentT-LymphocytesMonophosphoryl Lipid ALipid Achemistry.chemical_compoundImmunology and InflammationImmune systemAdjuvants ImmunologicInterferonTLRmedicineHumansprimary human cellsAgedImmunity CellularToll-like receptorMultidisciplinarySARS-CoV-2ChemistryToll-Like ReceptorsImidazolesCOVID-19Dendritic CellsTLR7biochemical phenomena metabolism and nutritionBiological SciencesMiddle AgedCOVID-19 ; TLR ; primary human cells ; adjuvants ; mRNA vaccines420Cell biologymRNA vaccinesLipid AadjuvantsTLR4[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleResiquimodmedicine.drugProceedings of the National Academy of Sciences
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Budesonide increases TLR4 and TLR2 expression in Treg lymphocytes of allergic asthmatics

2015

Abstract Background Reduced innate immunity responses as well as reduced T regulatory activities characterise bronchial asthma. Objectives In this study the effect of budesonide on the expression of TLR4 and TLR2 in T regulatory lymphocyte sub-population was assessed. Methods TLR4 and TLR2 expression in total peripheral blood mononuclear cells (PBMC), in CD4+/CD25+ and in CD4+/CD25− was evaluated, by flow cytometric analysis, in mild intermittent asthmatics (n = 14) and in controls (n = 11). The in vitro effects of budesonide in modulating: TLR4 and TLR2 expression in controls and in asthmatics; IL-10 expression and cytokine release (IL-6 and TNF-α selected by a multiplex assay) in asthmati…

AdultMalePulmonary and Respiratory MedicineBudesonidemedicine.medical_treatmentLymphocyteIn Vitro TechniquesCorticosteroids; Immunoregulation; T lymphocytes; TLR; Adult; Asthma; Budesonide; Cytokines; Female; Flow Cytometry; Glucocorticoids; Humans; In Vitro Techniques; Interleukin-10; Leukocytes Mononuclear; Male; T-Lymphocytes Regulatory; Toll-Like Receptor 2; Toll-Like Receptor 4; Young Adult; Pulmonary and Respiratory Medicine; Pharmacology (medical); Biochemistry (medical); Medicine (all)T-Lymphocytes RegulatoryPeripheral blood mononuclear cellYoung AdultGlucocorticoidTLRT lymphocytemedicineCorticosteroidHumansPharmacology (medical)IL-2 receptorBudesonideCytokineGlucocorticoidsIn Vitro Techniquebusiness.industryMedicine (all)Biochemistry (medical)ImmunoregulationFlow CytometryAsthmaToll-Like Receptor 2Interleukin-10Toll-Like Receptor 4Interleukin 10TLR2Cytokinemedicine.anatomical_structureImmunologyLeukocytes MononuclearTLR4CytokinesFemalebusinessHumanmedicine.drugPulmonary Pharmacology & Therapeutics
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