Search results for "TLR2"

showing 10 items of 57 documents

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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TLR2 modulates gut colonization and dissemination of Candida albicans in a murine model

2016

Invasive candidiasis often arises from translocation of endogenous yeasts from the gastrointestinal tract to the bloodstream. Here we describe that both wild type and TLR2−/− mice strains, orally administered with Candida albicans yeasts, display similar sustained high level of gut colonization when oral antibacterial treatment is present, while removal of antibiotic treatment causes a progressive clearance of yeasts in control but not in TLR2−/− mice. Fungal invasion of internal organs, following immunosuppression of colonized mice, was increased in TLR2−/− mice. These results point out to a role of TLR2 in gut protection against colonization and endogenous invasion by C. albicans. This wo…

0301 basic medicinemedicine.drug_classFarmacología030106 microbiologyImmunologyAntibioticsEndogenyGut colonizationMicrobiologyMicrobiology03 medical and health sciencesImmunosuppressed miceCandida albicansmedicineTLR2AnimalsCandidiasis InvasiveColonizationCandida albicansMice KnockoutGastrointestinal tractbiologyWild typebiology.organism_classificationToll-Like Receptor 2Corpus albicansGastrointestinal TractMice Inbred C57BLTLR2030104 developmental biologyInfectious DiseasesImmunologyDisease SusceptibilityMicrobes and Infection
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The switch from proteasome to immunoproteasome is increased in circulating cells of patients with fast progressive immunoglobulin A nephropathy and a…

2021

  The proteasome to immunoproteasome (iPS) switch consists of β1, β2 and β5 subunit replacement by low molecular weight protein 2 (LMP2), LMP7 and multicatalytic endopeptidase-like complex-1 (MECL1) subunits, resulting in a more efficient peptide preparation for major histocompatibility complex 1 (MHC-I) presentation. It is activated by toll-like receptor (TLR) agonists and interferons and may also be influenced by genetic variation. In a previous study we found an iPS upregulation in peripheral cells of patients with immunoglobulin A nephropathy (IgAN). We aimed to investigate in 157 IgAN patients enrolled through the multinational Validation Study of the Oxford Classification of IgAN (VAL…

0301 basic medicinemedicine.medical_specialtyProteasome Endopeptidase Complex030232 urology & nephrologyCD46; IgA nephropathy; biomarkers; complement; immune proteasome; progression; risk factorsMajor histocompatibility complexMembrane Cofactor Protein03 medical and health sciences0302 clinical medicineDownregulation and upregulationInternal medicinemedicinerisk factorsHumanscomplementRNA MessengerReceptorCD46Transplantationmedicine.diagnostic_testbiologybusiness.industrybiomarkersPSMB8Glomerulonephritis IGAIgA nephropathyPSMB9medicine.diseaseUp-RegulationTLR2030104 developmental biologyEndocrinologyNephrologybiology.proteinprogressionRenal biopsyimmune proteasomebusinessKidney diseaseGenome-Wide Association StudyNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
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Filifactor alocis and Tumor Necrosis Factor-Alpha Stimulate Synthesis of Visfatin by Human Macrophages

2021

There is little known about the effect of the periodontopathogen Filifactor alocis on macrophages as key cells of the innate immune defense in the periodontium. Therefore, the aim of the present study was to investigate the effect of F. alocis and additionally of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF&alpha

0301 basic medicinemedicine.medical_treatmentCD14tumor necrosis factor<i>Filifactor alocis</i>610 Medicine & healthmacrophageArticleCatalysisProinflammatory cytokineInorganic Chemistrylcsh:Chemistry03 medical and health sciences0302 clinical medicinestomatognathic systemvisfatinmedicineMacrophagePhysical and Theoretical Chemistry610 Medicine &amp; healthMolecular Biologyperiodontitislcsh:QH301-705.5SpectroscopyPeriodontitisInnate immune systembusiness.industryOrganic Chemistry030206 dentistryGeneral Medicinemedicine.diseaseComputer Science ApplicationsFilifactor alocisTLR2030104 developmental biologyCytokinelcsh:Biology (General)lcsh:QD1-999ImmunologyTumor necrosis factor alphaMMP1businessCOX2International Journal of Molecular Sciences
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PRR signaling during in vitro macrophage differentiation from progenitors modulates their subsequent response to inflammatory stimuli.

2017

Toll-like receptor (TLR) agonists drive hematopoietic stem and progenitor cells (HSPCs) to differentiate along the myeloid lineage in vitro and also in vivo following infection. In this study, we used an in vitro model of HSPC differentiation to investigate the functional consequences (cytokine production) that exposing HSPCs to various pathogen-associated molecular patterns (PAMPs) and Candida albicans cells have on the subsequently derived macrophages. Mouse HSPCs (Lin- cells) were cultured with GM-CSF to induce macrophage differentiation in the presence or absence of the following pattern recognition receptor (PRR) agonists: Pam3CSK4 (TLR2 ligand), LPS (TLR4 ligand), depleted zymosan (wh…

0301 basic medicinemedicine.medical_treatmentClinical BiochemistryImmunologyProinflammatory cytokineMajor Histocompatibility Complex03 medical and health scienceschemistry.chemical_compoundMicemedicineEscherichia coliImmunology and AllergyAnimalsAntigens LyProgenitor cellCells CulturedChemistryMacrophagesZymosanPattern recognition receptorCell DifferentiationFlow CytometryCell biologyMice Inbred C57BLHaematopoiesisTLR2030104 developmental biologyCytokineReceptors Pattern RecognitionTLR4CytokinesFemaleSignal TransductionEuropean cytokine network
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Immunosuppression, peripheral inflammation and invasive infection from endogenous gut microbiota activate retinal microglia in mouse models

2016

Although its actual role in the progression of degenerative processes is not fully known, the persistent activated state of retinal microglia and the concurrent secretion of inflammatory mediators may contribute to neuronal death and permanent vision loss. Our objective was to determine whether non-ocular conditions (immunosuppression and peripheral inflammation) could lead to activation of retinal microglia. Mouse models of immunosuppression induced by cyclophosphamide and/or peripheral inflammation by chemically induced sublethal colitis in C57BL/6J mice were used. Retinal microglia morphology, spatial distribution and complexity, as well as MHCII and CD11b expression levels were determin…

0301 basic medicinemedicine.medical_treatmentImmunologyInflammationMicrobiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationVirologymedicineColitisMicrogliabiologyImmunosuppressionRetinalmedicine.diseaseTLR2030104 developmental biologymedicine.anatomical_structureIntegrin alpha MchemistryImmunologybiology.proteinmedicine.symptom030217 neurology & neurosurgeryMicrobiology and Immunology
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TLR2 and age-related diseases: potential effects of Arg753Gln and Arg677Trp polymorphisms in acute myocardial infarction.

2008

ABSTRACT Inflammation is a key component of immune system. It is involved in both defense and pathophysiological events maintaining the dynamic homeostasis of host organism. Its function is controlled by innate immunity genes. Both their polymorphisms and environmental conditions give rise to different phenotypes in human population. Proinflammatory genotype may be beneficial in early life but not in old people. With advancing age, indeed, it increases the vulnerability and the intensity to inflammatory reactions responsible for the chronic inflammatory diseases, such as atherosclerosis and myocardial infarction (MI). Several studies have looked for detecting a genetic risk profile that mig…

AdultAgingSettore MED/09 - Medicina InternaGenotypePopulationMyocardial InfarctionInflammationPolymorphism Single NucleotideProinflammatory cytokineImmune systemGene FrequencyMedicineHumansMyocardial infarctioneducationSettore MED/04 - Patologia Generaleeducation.field_of_studyInnate immune systembusiness.industryMiddle Agedmedicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareToll-Like Receptor 2TLR2Amino Acid SubstitutionItalyTLR2age-related diseasespolymorphismsacute myocardial infarction.PharmacogenomicsCase-Control StudiesImmunologyGeriatrics and Gerontologymedicine.symptombusinessRejuvenation research
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In vitroresponse toCandida albicansin cultures of whole human blood from young and aged donors

2007

Invasive infections with opportunistic fungi, such as Candida albicans, have become an increasing problem in aged adults in recent years. This work investigates the influence of human ageing on C. albicans recognition by toll-like receptors (TLRs), essential components of the innate immune system, using a cohort of 96 young (15-42 years) and aged (70 years) human volunteers. No significant differences between aged and young donors were observed on (1) cell surface TLR2, TLR6 and TLR4 expression on lymphocytes, monocytes and granulocytes, (2) production of cytokines [IL-8, IL-1beta, IL-6, IL-10, tumour necrosis factor (TNF)-alpha and IL-12p70] and prostaglandin E(2) (PGE(2)) by whole human b…

AdultMaleMicrobiology (medical)Adolescentmedicine.medical_treatmentImmunologyBiologyMicrobiologyDinoprostoneMonocytesCandida albicansmedicineHumansImmunology and AllergyBlood cultureLymphocytesCandida albicansAntibodies FungalAgedWhole bloodAged 80 and overMicrobial ViabilityInnate immune systemmedicine.diagnostic_testAge FactorsGeneral Medicinebiology.organism_classificationToll-Like Receptor 2Corpus albicansToll-Like Receptor 4TLR2BloodToll-Like Receptor 6Infectious DiseasesCytokineImmunologybiology.proteinCytokinesFemaleAntibodyGranulocytesFEMS Immunology &amp; Medical Microbiology
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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 &amp; Therapeutics
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Cancer relapse under chemotherapy: why TLR2/4 receptor agonists can help.

2007

Liver or lung metastases usually relapse under chemotherapy. Such life-threatening condition urgently needs new, systemic anticancer compounds, with original and efficient mechanisms of action. In B16 melanoma mice treated with cyclophosphamide, D'Agostini et al. [D'Agostini, C., Pica, F., Febbraro, G., Grelli, S., Chiavaroli, C., Garaci, E., 2005. Antitumour effect of OM-174 and Cyclophosphamide on murine B16 melanoma in different experimental conditions. Int. Immunopharmacol. 5, 1205-1212.] recently found that OM-174, a chemically defined Toll-like receptor(TLR)2/4 agonist, reduces tumor progression and prolongs survival. Here we review 149 articles concerning molecular mechanisms of TLR2…

AgonistLipopolysaccharidesCyclophosphamidemedicine.drug_classmedicine.medical_treatmentNitric Oxide Synthase Type IIAntineoplastic AgentsApoptosisNitric oxidechemistry.chemical_compoundRecurrenceNeoplasmsMedicineAnimalsHumansPharmacologyChemotherapybusiness.industryTumor Necrosis Factor-alphaCancerDendritic Cellsmedicine.diseaseNeoadjuvant TherapyToll-Like Receptor 2Interleukin-10Toll-Like Receptor 4TLR2Lipid ATreatment OutcomechemistryTumor progressionChemotherapy AdjuvantDrug Resistance NeoplasmEnzyme InductionImmunologyCancer researchBCG VaccineTumor necrosis factor alphaImmunotherapybusinessmedicine.drugSignal TransductionT-Lymphocytes CytotoxicEuropean journal of pharmacology
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