Search results for "immune"

showing 10 items of 3935 documents

Impact of fascioliasis reinfection on Fasciola hepatica egg shedding: relationship with the immune-regulatory response.

2019

Abstract Fascioliasis is a disease caused by liver flukes. In human fascioliasis hyperendemic areas, reinfection and chronicity are the norm. Control strategies in humans require the use of egg count techniques to calculate the appropriate treatment dose for colic risk prevention. The present study investigates how fascioliasis reinfection affects liver fluke egg shedding and its relationship with the immune-regulatory response. The experimental design reproduced the usual reinfection/chronicity conditions in human fascioliasis endemic areas and included Fasciola hepatica primo-infected Wistar rats (PI) and rats reinfected at 4 weeks (R4), 8 weeks (R8), 12 weeks (R12), and negative control …

0301 basic medicineMaleFascioliasisVeterinary (miscellaneous)030231 tropical medicinePhysiologySpleenBiology03 medical and health sciences0302 clinical medicineImmune systemRecurrenceparasitic diseasesmedicineFasciola hepaticaAnimalsLongitudinal StudiesRats WistarParasite Egg CountEggs per gramFecesFOXP3030108 mycology & parasitologyLiver flukeFasciola hepaticabiology.organism_classificationInterleukin-10RatsInterleukin 10Infectious Diseasesmedicine.anatomical_structureCross-Sectional StudiesInsect ScienceImmunoglobulin GParasitologyActa tropica
researchProduct

The Commensal Microbiota Enhances ADP-Triggered Integrin αIIbβ3 Activation and von Willebrand Factor-Mediated Platelet Deposition to Type I Collagen

2020

The commensal microbiota is a recognized enhancer of arterial thrombus growth. While several studies have demonstrated the prothrombotic role of the gut microbiota, the molecular mechanisms promoting arterial thrombus growth are still under debate. Here, we demonstrate that germ-free (GF) mice, which from birth lack colonization with a gut microbiota, show diminished static deposition of washed platelets to type I collagen compared with their conventionally raised (CONV-R) counterparts. Flow cytometry experiments revealed that platelets from GF mice show diminished activation of the integrin αIIbβ3 (glycoprotein IIbIIIa) when activated by the platelet agonist adenosine diphosphate (ADP). Fu…

0301 basic medicineMaleGene Expression030204 cardiovascular system & hematologyvon Willebrand factorlcsh:Chemistrychemistry.chemical_compoundMice0302 clinical medicinePlateletToll-like receptor-2lcsh:QH301-705.5SpectroscopyMice KnockoutbiologyChemistryBrief ReportαIIbβ3General MedicineArteriesComputer Science ApplicationsCell biologyAdenosine DiphosphatePlatelet Glycoprotein GPIb-IX Complexgerm-freeplateletsFemaleType I collagenBlood PlateletsIntegrinPrimary Cell CulturePlatelet Glycoprotein GPIIb-IIIa ComplexCatalysisCollagen Type IInorganic Chemistry03 medical and health sciencesVon Willebrand factormedicineCell AdhesionmicrobiotaAnimalsGerm-Free LifeHumansPhysical and Theoretical ChemistryThrombusSymbiosisMolecular Biologyα<sub>IIb</sub>β<sub>3</sub>Innate immune systemOrganic ChemistryThrombosismedicine.diseaseImmunity InnateToll-Like Receptor 2Gastrointestinal MicrobiomeMice Inbred C57BLAdenosine diphosphateTLR2030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinInternational Journal of Molecular Sciences
researchProduct

Disease severity in patients with visceral leishmaniasis is not altered by co-infection with intestinal parasites

2017

Visceral leishmaniasis (VL) is a neglected tropical disease that affects the poorest communities and can cause substantial morbidity and mortality. Visceral leishmaniasis is characterized by the presence of Leishmania parasites in the spleen, liver and bone marrow, hepatosplenomegaly, pancytopenia, prolonged fever, systemic inflammation and low body mass index (BMI). The factors impacting on the severity of VL are poorly characterized. Here we performed a cross-sectional study to assess whether co-infection of VL patients with intestinal parasites influences disease severity, assessed with clinical and haematological data, inflammation, cytokine profiles and BMI. Data from VL patients was s…

0301 basic medicineMaleIMPACTPhysiologyHepatosplenomegalySystemic inflammationPathology and Laboratory MedicineTHERAPYSeverity of Illness IndexBody Mass Index0302 clinical medicineIntestinal ParasitesBone MarrowZoonosesImmune PhysiologyMedicine and Health SciencesIntestinal Diseases ParasiticHELMINTH INFECTIONSLeishmaniasisImmune ResponseInnate Immune SystembiologyCoinfectionlcsh:Public aspects of medicineASCARIASIS11 Medical And Health SciencesHematologyPancytopenia3. Good healthInfectious DiseasesCytokinesLeishmaniasis Visceralmedicine.symptomLife Sciences & BiomedicineHepatomegalyResearch ArticleNeglected Tropical DiseasesAdultlcsh:Arctic medicine. Tropical medicineAdolescentlcsh:RC955-962030231 tropical medicineImmunology03 medical and health sciencesYoung AdultSigns and SymptomsDONOVANIDiagnostic MedicineTropical MedicineHOOKWORMSeverity of illnessmedicineParasitic DiseasesAnimalsHumansParasitesInflammationScience & TechnologyProtozoan InfectionsINTERFERON-GAMMAbusiness.industryPublic Health Environmental and Occupational HealthTropical diseaseBiology and Life SciencesLeishmaniasislcsh:RA1-127006 Biological SciencesMolecular DevelopmentINTERLEUKIN-10Leishmaniabiology.organism_classificationmedicine.diseaseTropical Diseases030104 developmental biologyVisceral leishmaniasisCross-Sectional StudiesLogistic ModelsCase-Control StudiesCo-InfectionsImmune SystemImmunologySplenomegalyUNDERNUTRITIONParasitologyEthiopiabusinessParasitic Intestinal DiseasesSpleenDevelopmental Biology
researchProduct

Plasmacytoid dendritic cells promote systemic sclerosis with a key role for TLR8

2018

Systemic sclerosis (SSc) is a multisystem life-threatening fibrosing disorder that lacks effective treatment. The link between the inflammation observed in organs such as the skin and profibrotic mechanisms is not well understood. The plasmacytoid dendritic cell (pDC) is a key cell type mediating Toll-like receptor (TLR)-induced inflammation in autoimmune disease patients, including lupus and skin diseases with interface dermatitis. However, the role of pDCs in fibrosis is less clear. We show that pDCs infiltrate the skin of SSc patients and are chronically activated, leading to secretion of interferon-α (IFN-α) and CXCL4, which are both hallmarks of the disease. We demonstrate that the s…

0301 basic medicineMaleInflammationPlasmacytoid dendritic cellPlatelet Factor 4SclerodermaArticlePathogenesis03 medical and health sciencesBleomycinMice0302 clinical medicineFibrosismedicineAnimalsHumansSkin030203 arthritis & rheumatologyAutoimmune diseaseSystemic lupus erythematosusScleroderma Systemicintegumentary systembusiness.industryMedicine (all)Interferon-alphahemic and immune systemsGeneral MedicineTLR7Dendritic CellsMiddle Agedmedicine.diseaseFibrosisDisease Models Animal030104 developmental biologyToll-Like Receptor 7Toll-Like Receptor 8ImmunologyFemalemedicine.symptombusinessSignal Transduction
researchProduct

Increased PD-1 Expression and Altered T Cell Repertoire Diversity Predict Mortality in Patients with Septic Shock: A Preliminary Study

2017

Sepsis causes impairment of innate and adaptive immunity by multiple mechanisms, including depletion of immune effector cells and T cell exhaustion. Although lymphocyte dysfunction is associated with increased mortality and potential reactivation of latent viral infection in patients with septic shock, the relation between viral reactivation and lymphocyte dysfunction is obscure. The objectives of this study were 1) to determine the relation of lymphocyte dysfunction to viral reactivation and mortality, and 2) to evaluate recovery of lymphocyte function during septic shock, including T cell receptor (TCR) diversity and the expression of programmed death 1 (PD-1). In 18 patients with septic …

0301 basic medicineMaleLymphocyteReceptor expressionProgrammed Cell Death 1 Receptorlcsh:MedicineCytomegalovirusGene ExpressionArtificial Gene Amplification and ExtensionPathology and Laboratory MedicineImmune ReceptorsBiochemistryPolymerase Chain ReactionMonocytesWhite Blood Cells0302 clinical medicineSpectrum Analysis TechniquesAnimal CellsT-Lymphocyte SubsetsMedicine and Health SciencesLymphocyteslcsh:ScienceAged 80 and overMultidisciplinaryImmune System ProteinsT CellsMiddle AgedAcquired immune systemFlow CytometryPrognosisShock Septicmedicine.anatomical_structurePhenotypeSpectrophotometryShock (circulatory)Cytomegalovirus InfectionsFemaleCytophotometrymedicine.symptomCellular TypesResearch ArticleSignal TransductionT cellImmune CellsImmunologyReceptors Antigen T-CellBiologyResearch and Analysis MethodsMicrobiologyImmunophenotypingSepsis03 medical and health sciencesImmune systemSigns and SymptomsDiagnostic MedicineSepsisVirologymedicineHumansMolecular Biology TechniquesMolecular BiologyAgedBlood CellsSeptic shocklcsh:RBiology and Life SciencesProteins030208 emergency & critical care medicineCell BiologyHLA-DR Antigensmedicine.diseaseViral ReplicationT Cell Receptors030104 developmental biologyCase-Control StudiesImmunologylcsh:QBiomarkersPLoS ONE
researchProduct

Social stress during adolescence activates long-term microglia inflammation insult in reward processing nuclei

2018

The experience of social stress during adolescence is associated with higher vulnerability to drug use. Increases in the acquisition of cocaine self-administration, in the escalation of cocaine-seeking behavior, and in the conditioned rewarding effects of cocaine have been observed in rodents exposed to repeated social defeat (RSD). In addition, prolonged or severe stress induces a proinflammatory state with microglial activation and increased cytokine production. The aim of the present work was to describe the long-term effects induced by RSD during adolescence on the neuroinflammatory response and synaptic structure by evaluating different glial and neuronal markers. In addition to an inc…

0301 basic medicineMaleMacroglial CellsHippocampuslcsh:MedicineSocial SciencesCell CountPathology and Laboratory MedicineHippocampusSocial defeatMice0302 clinical medicineCocaineAnimal CellsConditioning PsychologicalMedicine and Health SciencesPsychologylcsh:ScienceImmune ResponseNeuronsMultidisciplinaryMicrogliaAnimal BehaviorBrainChemistrymedicine.anatomical_structureBehavioral PharmacologyAnimal SocialityPhysical SciencesMicrogliamedicine.symptomCellular TypesAnatomyResearch ArticleInfralimbic cortexImmunologyPsychological StressInflammationGlial CellsNucleus accumbensProinflammatory cytokine03 medical and health sciencesAlkaloidsSigns and SymptomsRewardDiagnostic MedicineRecreational Drug UseMental Health and PsychiatrymedicineAnimalsMicroglial CellsSocial stressPharmacologyInflammationBehaviorbusiness.industrylcsh:RChemical CompoundsBiology and Life SciencesCell Biology030104 developmental biologyAstrocytesCellular Neurosciencelcsh:QbusinessNeuroscienceZoology030217 neurology & neurosurgeryStress PsychologicalNeuroscience
researchProduct

MICA-129 Dimorphism and Soluble MICA Are Associated With the Progression of Multiple Myeloma

2018

Natural killer (NK) cells are immune innate effectors playing a pivotal role in the immunosurveillance of multiple myeloma (MM) since they are able to directly recognize and kill MM cells. In this regard, among activating receptors expressed by NK cells, NKG2D represents an important receptor for the recognition of MM cells, being its ligands expressed by tumor cells, and being able to trigger NK cell cytotoxicity. The MHC class I-related molecule A (MICA) is one of the NKG2D ligands; it is encoded by highly polymorphic genes and exists as membrane-bound and soluble isoforms. Soluble MICA (sMICA) is overexpressed in the serum of MM patients, and its levels correlate with tumor progression. …

0301 basic medicineMaleModels MolecularProtein ConformationGenotypeImmunology and AllergyReceptorpredictive biomarkerOriginal ResearchAged 80 and overnatural killer cellsbiologyChemistryMiddle AgedImmunosurveillanceGene Expression Regulation NeoplasticKiller Cells Naturalmultiple myelomaNK Cell Lectin-Like Receptor Subfamily KDisease ProgressionFemaleNKG2D receptorProtein Bindinglcsh:Immunologic diseases. AllergyGenotypeImmunologyEnzyme-Linked Immunosorbent AssayMICA polymorphismImmunophenotyping03 medical and health sciencesStructure-Activity RelationshipImmune systemMHC class IHumansGenetic Predisposition to DiseaseAllelesGenetic Association StudiesAgedPolymorphism GeneticHistocompatibility Antigens Class INKG2DMolecular biologyMolecular Typingstomatognathic diseases030104 developmental biologyAmino Acid SubstitutionTumor progressionbiology.proteinmultiple myeloma natural killer cells NKG2D receptor MICA polymorphism predictive biomarkerGene polymorphismlcsh:RC581-607Frontiers in Immunology
researchProduct

Odiparcil, a potential glycosaminoglycans clearance therapy in mucopolysaccharidosis VI—Evidence from in vitro and in vivo models

2020

International audience; Mucopolysaccharidoses are a class of lysosomal storage diseases, characterized by enzymatic deficiency in the degradation of specific glycosaminoglycans (GAG). Pathological accumulation of excess GAG leads to multiple clinical symptoms with systemic character, most severely affecting bones, muscles and connective tissues. Current therapies include periodic intravenous infusion of supplementary recombinant enzyme (Enzyme Replacement Therapy-ERT) or bone marrow transplantation. However, ERT has limited efficacy due to poor penetration in some organs and tissues. Here, we investigated the potential of the β-D-xyloside derivative odiparcil as an oral GAG clearance therap…

0301 basic medicineMaleMucopolysaccharidosis type VIRespiratory SystemAdministration OralGlycosaminoglycanRats Sprague-DawleyWhite Blood CellsMice0302 clinical medicineOral administrationAnimal CellsMedicine and Health SciencesGlycosidesCells CulturedConnective Tissue CellsGlycosaminoglycansMultidisciplinaryMucopolysaccharidosis VIChemistryChondroitin SulfatesQRMucopolysaccharidosis VIAnimal Models3. Good healthTracheamedicine.anatomical_structureExperimental Organism SystemsConnective Tissue[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyMedicineFemaleBiological CulturesCellular TypesAnatomyCellular Structures and OrganellesResearch Articlemedicine.medical_specialtyImmune CellsScienceImmunologyDermatan SulfateMouse ModelsIn Vitro TechniquesResearch and Analysis Methods03 medical and health sciencesModel OrganismsIn vivoInternal medicinemedicineAnimalsHumansBlood CellsCartilageBiology and Life SciencesEndothelial CellsKidneysCell BiologyRenal SystemFibroblastsCell CulturesIn vitroMice Mutant StrainsRatsMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyBiological TissueCartilageCell cultureAnimal Studies[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyCattleLysosomes030217 neurology & neurosurgery
researchProduct

Transcriptome Analysis Identifies Doublesex and Mab-3 Related Transcription Factor (DMRT3) in Nasal Polyp Epithelial Cells of Patients Suffering from…

2021

Background: Aspirin-exacerbated respiratory disease (AERD) is a syndrome characterised by chronic rhinosinusitis, nasal polyps, asthma and aspirin intolerance. An imbalance of eicosanoid metabolism with anover-production of cysteinyl leukotrienes (CysLTs) has been associated with AERD. However, the precise mechanisms underlying AERD are unknown. Objective: To establish the transcriptome of the nasal polyp airway epithelial cells derived from AERD patients to discover gene expression patterns in this disease. Methods: Nasal airway epithelial cells were isolated from 12 AERD polyps and 8 AERD non-polyp nasal mucosa samples as controls from the same subjects. Utilising the Illumina HiSeq 2500 …

0301 basic medicineMaleMucous membrane of noseBiochemistryDMRT3TranscriptomeTranscription Factors TFII0302 clinical medicinetranscriptome analysisGene expressionMedicineNasal polypsRNA-SeqEicosanoid metabolismAnti-Inflammatory Agents Non-SteroidalMiddle AgedImmunohistochemistryQR1-502030220 oncology & carcinogenesisImmunohistochemistryFemalemedicine.symptomAdultLeukotrienesAspirin-exacerbated respiratory diseaseInflammationMicrobiologyArticle03 medical and health sciencesImmune systemNasal Polypsotorhinolaryngologic diseasesHumansSinusitisMolecular BiologySkin TestsAspirinbusiness.industryGene Expression Profilingnasal airwayEpithelial Cellsmedicine.diseaseRespiration Disorders030104 developmental biologyImmunologyChronic DiseaseNasal LavageAsthma Aspirin-InducedbusinessTranscriptomeBiomolecules
researchProduct

Characterization of the Clinical and Immunologic Phenotype and Management of 157 Individuals with 56 Distinct Heterozygous NFKB1 Mutations

2020

Contains fulltext : 229571.pdf (Publisher’s version ) (Closed access) BACKGROUND: An increasing number of NFKB1 variants are being identified in patients with heterogeneous immunologic phenotypes. OBJECTIVE: To characterize the clinical and cellular phenotype as well as the management of patients with heterozygous NFKB1 mutations. METHODS: In a worldwide collaborative effort, we evaluated 231 individuals harboring 105 distinct heterozygous NFKB1 variants. To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling. RESU…

0301 basic medicineMaleNF-KAPPA-BMedizinlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Fluorescent Antibody TechniqueAutoimmunityDiseaseNUCLEAR-FACTORKaplan-Meier Estimatemedicine.disease_causeHypogammaglobulinemia0302 clinical medicineNFKB1 variants and mutations; autosomal dominant inheritance; common variable immunodeficiency; reduced penetrance; variable expressivityHDE PEDImmunology and Allergyvariants and mutationsNF-κB1-related phenotypeImmunodeficiencyIMMUNODEFICIENCY*NF-?B1-related phenotypeNFKB1 variants and mutations1184 Genetics developmental biology physiologycommon variable immunodeficiencyDisease ManagementMiddle AgedNF-kappa B1-related phenotypereduced penetrancePrognosisPenetranceImmunohistochemistryMagnetic Resonance Imaging3. Good healthPhenotypeNFKB1 variant*NFKB1 variant*common variable immunodeficiencyFemaleHaploinsufficiency*reduced penetranceNFKB1 mutationAdultHeterozygote*NFKB1 mutationImmunologyHAPLOINSUFFICIENCYArticle03 medical and health sciencesvariable expressivityautosomal dominantmedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesAgedbusiness.industryCommon variable immunodeficiencyNF-kappa B p50 SubunitNF-KAPPA-B1Immune dysregulationmedicine.diseaseautosomal dominant inheritance030104 developmental biologyBiological Variation PopulationImmunologyCELLSMutation*autosomal dominantPrimary immunodeficiency3111 BiomedicinebusinessTomography X-Ray ComputedBiomarkers030215 immunology
researchProduct