Search results for "toll"

showing 10 items of 324 documents

SARS CoV2 infection _The longevity study perspectives

2021

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MaleAgingssRNA single-stranded RNARFLP restriction fragment length polymorphismHSPs heat shock proteinsReviewPTMs post-translational modificationsSevere Acute Respiratory SyndromeBiochemistryHIV-1 human immunodeficiency virus-1TNF-α tumor necrosis factor-αEC endothelial cells0302 clinical medicineFluAV influenza A virusI insertionMedicineIFN-γ interferon-γDIC disseminated intravascular coagulationPCR Polymerase Chain Reactionmedia_commonAged 80 and overLongevityRBD receptor-binding domainNeurologyLongevity modelMI myocardial infarctionNK natural killerhPIV2 human parainfluenza virus type 2media_common.quotation_subjectResearching genetic basis of resistance and potential pharmacological targetsLongevityDBP diastolic blood pressureNF-Kb nuclear transcription factor kBRANTES regulated upon activation normal T cell expressed and secretedMphi human macrophages03 medical and health sciencesCox 2 cyclooxygenase 2ORF open reading framePT prothrombin timeSettore MED/05 - Patologia ClinicaHumansMolecular BiologyInflammatory genesARDS acute respiratory distress syndromeNO nitric oxideD deletionCpGIs CpG islandsT2DM type 2 diabetes mellitusmedicine.diseaseFDP fibrin degradation products030104 developmental biologySARS CoV2 severe acute respiratory syndrome Coronavirus 2 virusImmunologyBMI body max indexItalian nonagenarians/centenariansRSV respiratory syncytial virusComplication030217 neurology & neurosurgeryMAPK mitogen-activated protein kinaseIP-10 IFN-γ -Inducible Protein 1040301 basic medicineAT1R activity of angiotensin 1 receptorsDCs dentritic cellsSSCP single strand conformation polymorphismACE/DD polymorphism of the angiotensin converting enzymeFGF21 fibroblast growth factor 21TLR4 toll-like receptor 4NAD nicotinamide adenine dinucleotideACE angiotensin-I converting enzymeAT2R activity of angiotensin 2 receptorsCOVID-19 Coronavirus disease 2019Respiratory distressACE2 angiotensin converting enzyme 2MKP-1 mitogen-activated protein kinase phosphatase-1 ()PD protease domainSNP single nucleotide polymorphismEH essential hypertensionTNFR tumor necrosis factor receptorINR international normalized ratio of the prothrombin timePAI-1 plasminogen activator inhibitor-1Ang angiotensinLPS lipopolysaccharideMCP1 monocyte chemoattractant protein-1medicine.symptomaPTT partial thromboplastin timeBiotechnologyDUSP1 dual specificity phosphatase 1Coronavirus disease 2019 (COVID-19)PC prostate cancerRAS renin-angiotensin aldosterone systemCCR5Δ32 genetic variant of chemokine receptorCOVID-19 Researching genetic basis of resistance and potential pharmacological targets Italian nonagenarians/centenarians Longevity modelAsymptomaticSARS-1 severe acute respiratory syndrome virus 1SIRT-1 Sirtuin 1Th1 t-helper lymphocyte type 1Immune systemROS reactive oxygen speciesTGF-β transforming growth factor betaET-1 endothelin-1ComputingMethodologies_COMPUTERGRAPHICSADAM-17 metallopeptidase domain 17business.industrySARS-CoV-2SBP systolic blood pressureCOVID-19HDACs histone deacetylasesComorbidityImmune Systembusiness5-LO lipoxygenase 5Ageing Research Reviews
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Can the TLR-4-mediated signaling pathway be "a key inflammatory promoter for sporadic TAA"?

2014

Thoracic aorta shows with advancing age various changes and a progressive deterioration in structure and function. As a result, vascular remodeling (VR) and medial degeneration (MD) occur as pathological entities responsible principally for the sporadic TAA onset. Little is known about their genetic, molecular, and cellular mechanisms. Recent evidence is proposing the strong role of a chronic immune/inflammatory process in their evocation and progression. Thus, we evaluated the potential role of Toll like receptor- (TLR-) 4-mediated signaling pathway and its polymorphisms in sporadic TAA. Genetic, immunohistochemical, and biochemical analyses were assessed. Interestingly, the rs4986790 TLR4…

MaleArticle SubjectGenotypeImmunologyAortic DiseasesSettore MED/41 - AnestesiologiaSingle-nucleotide polymorphismAorta ThoracicSettore MED/08 - Anatomia PatologicaBiologyPolymorphism Single NucleotideImmune systemPolymorphism (computer science)Genotypelcsh:PathologySettore MED/05 - Patologia ClinicaHumansGenetic Predisposition to DiseaseAgedToll-like receptorPolymorphism GeneticSettore MED/23 - Chirurgia CardiacaCell BiologyMiddle AgedPhenotypeImmunohistochemistryToll-Like Receptor 4medial degeneration sporadic thoracic aortic aneurysm TLR-4 mediated signaling pathway rs4986790 TLR4 polymorphism translation of genetic immunohistochemical and biochemical data clinical practiceImmunologyTLR4Matrix Metalloproteinase 2FemaleSignal transductionlcsh:RB1-214Research ArticleSignal Transduction
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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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Molecular basis of endothelial dysfunction in sepsis.

2003

Sepsis is one of the major causes of mortality in critically ill patients and develops as a result of the host response to infection. A complex network of events is set into motion in the body by the infection and results in the pathogenesis of sepsis. This review article focuses on the molecular mechanisms and components involved in the pathogenesis of sepsis with a major emphasis on the endothelium. This includes sepsis-inducing bacterial components (e.g. endotoxins), cellular targets of these molecules and their responses, host reactions, intracellular and cytokine networks, individual susceptibility and new therapeutic targets in sepsis treatment.

MaleEndotheliumPhysiologymedicine.medical_treatmentReceptors Cell SurfaceBiologyNitric OxidePathogenesisSepsisPhysiology (medical)SepsismedicineHumansEndothelial dysfunctionHypoxiaMembrane GlycoproteinsToll-Like ReceptorsEndothelial Cellsmedicine.diseaseReview articleBacterial adhesinEndotoxinsmedicine.anatomical_structureCytokineImmunologyMutationCytokinesFemaleDisease SusceptibilityEndothelium VascularCardiology and Cardiovascular MedicineReactive Oxygen SpeciesCell Adhesion MoleculesIntracellularInterleukin-1Cardiovascular research
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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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