Search results for "interleukin"

showing 10 items of 1856 documents

Inflammasome activation in Ankylosing Spondylitis is associated to gut dysbiosis

2021

Objective: We undertook this study to evaluate the activation and functional relevance of inflammasome pathways in ankylosing spondylitis (AS) patients and rodent models and their relationship to dysbiosis. Methods: An inflammasome pathway was evaluated in the gut and peripheral blood from 40 AS patients using quantitative reverse transcriptase–polymerase chain reaction (qRT-PCR), immunohistochemistry (IHC), flow cytometry, and confocal microscopy, and was compared to that of 20 healthy controls and 10 patients with Crohn’s disease. Bacteria was visualized using silver stain in human samples, and antibiotics were administered to HLA–B27–transgenic rats. The NLRP3 inhibitor MCC950 was admini…

0301 basic medicineMaleInflammasomesmedicine.medical_treatmentInterleukin-1betaInterleukin-23Mice0302 clinical medicineCrohn DiseaseNLRC4Interleukin 23Immunology and AllergyIleitisHLA-B27 AntigenSulfonamidesReverse Transcriptase Polymerase Chain ReactionCaspase 1Interleukin-17Interleukin-18InflammasomeIleitisMiddle AgedImmunohistochemistryAnti-Bacterial AgentsDNA-Binding ProteinsCytokineIndenesFemaleInterleukin 17Rats Transgenicmedicine.drugAdultAdolescentImmunologyReceptors Cell Surface03 medical and health sciencesAIM2Young AdultRheumatologyIleumNLR Family Pyrin Domain-Containing 3 ProteinmedicineAnimalsHumansSpondylitis AnkylosingFurans030203 arthritis & rheumatologybusiness.industryCalcium-Binding Proteinsmedicine.diseaseGastrointestinal MicrobiomeRatsCARD Signaling Adaptor Proteins030104 developmental biologyCase-Control StudiesImmunologyDysbiosisJointsbusinessDysbiosis
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Chronic skin inflammation leads to bone loss by IL-17-mediated inhibition of Wnt signaling in osteoblasts

2016

Item does not contain fulltext Inflammation has important roles in tissue regeneration, autoimmunity, and cancer. Different inflammatory stimuli can lead to bone loss by mechanisms that are not well understood. We show that skin inflammation induces bone loss in mice and humans. In psoriasis, one of the prototypic IL-17A-mediated inflammatory human skin diseases, low bone formation and bone loss correlated with increased serum IL-17A levels. Similarly, in two mouse models with chronic IL-17A-mediated skin inflammation,K14-IL17A(ind)andJunB(Deltaep), strong inhibition of bone formation was observed, different from classical inflammatory bone loss where osteoclast activation leads to bone deg…

0301 basic medicineMaleInflammationModels BiologicalOsteocytesBone resorptionEpithelium03 medical and health sciences0302 clinical medicineOsteoclastOsteogenesismedicineAnimalsHumansPsoriasisCell LineageBone ResorptionWnt Signaling PathwaySkin030203 arthritis & rheumatologyInflammationOsteoblastsChemistryInnate lymphoid cellInterleukin-17Wnt signaling pathwayOsteoblastGeneral MedicineMiddle AgedMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression RegulationOsteocyteImmunologyChronic DiseaseCancer researchFemaleInterleukin 17medicine.symptomInflammatory diseases Radboud Institute for Molecular Life Sciences [Radboudumc 5]Science Translational Medicine
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Pistachio Consumption Alleviates Inflammation and Improves Gut Microbiota Composition in Mice Fed a High-Fat Diet.

2019

High-fat diet (HFD) induces inflammation and microbial dysbiosis, which are components of the metabolic syndrome. Nutritional strategies can be a valid tool to prevent metabolic and inflammatory diseases. The aim of the present study was to evaluate if the chronic intake of pistachio prevents obesity-associated inflammation and dysbiosis in HFD-fed mice. Three groups of male mice (four weeks old

0301 basic medicineMaleInterleukin-1betaAdipose tissueGut floralcsh:ChemistryMice0302 clinical medicineLactobacilluslcsh:QH301-705.5SpectroscopyChemokine CCL2biologydigestive oral and skin physiologyfood and beveragesGeneral Medicinepistachio intakeobesity-related inflammation pistachio intake gut microbiota HFD mice adipose tissueComputer Science Applicationsadipose tissueLiverPistacialipids (amino acids peptides and proteins)medicine.symptomhormones hormone substitutes and hormone antagonistsmedicine.medical_specialty030209 endocrinology & metabolismInflammationDiet High-FatCatalysisArticleInorganic Chemistry03 medical and health sciencesInternal medicineobesity-related inflammationmedicineAnimalsHFD miceObesityPhysical and Theoretical ChemistryMolecular BiologyFecesgut microbiotaTumor Necrosis Factor-alphaOrganic Chemistrynutritional and metabolic diseasesmedicine.diseasebiology.organism_classificationObesityGastrointestinal MicrobiomeMice Inbred C57BL030104 developmental biologyEndocrinologylcsh:Biology (General)lcsh:QD1-999DysbiosisMetabolic syndromeDysbiosisDiet TherapyInternational journal of molecular sciences
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Differential role of interleukin-1β in neuroinflammation-induced impairment of spatial and nonspatial memory in hyperammonemic rats.

2019

Activated microglia and increased brain IL-1β play a main role in cognitive impairment in much pathology. We studied the role of IL-1β in neuroinflammation-induced impairment of the following different types of learning and memory: novel object recognition (NOR), novel object location (NOL), spatial learning, reference memory (RM), and working memory (WM). All these processes are impaired in hyperammonemic rats. We assessed which of these types of learning and memory are restored by blocking the IL-1 receptor in vivo in hyperammonemic rats and the possible mechanisms involved. Blocking the IL-1 receptor reversed microglial activation in the hippocampus, perirhinal cortex, and prefrontal cor…

0301 basic medicineMaleInterleukin-1betaPostrhinal cortexHippocampusBiochemistryHippocampusReceptors N-Methyl-D-Aspartate03 medical and health sciences0302 clinical medicineReceptors GABAAmmoniaMemoryPerirhinal cortexGeneticsmedicineMemory impairmentAnimalsHyperammonemiaReceptors AMPARats WistarPrefrontal cortexMolecular BiologyNeuroinflammationCerebral CortexInflammationMicrogliabusiness.industryWorking memoryAnimal FeedRatsInterleukin 1 Receptor Antagonist ProteinProtein Subunits030104 developmental biologymedicine.anatomical_structureGene Expression RegulationReceptors GlutamateMicrogliabusinessNeuroscience030217 neurology & neurosurgeryBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Clinical response to non-surgical periodontal treatment in patients with interleukin-6 and interleukin-10 polymorphisms

2017

Background Genetic polymorphisms are commonly associated with altered transcriptional activity and possibly make individuals more susceptible to periodontal disease development, increased disease severity and poor treatment outcome. The study aimed to determine the effect of Interleukin-6 (IL-6) -572 G/C (rs1800796) and IL-10 -592 C/A (rs1800872) polymorphisms on the outcomes of non-surgical periodontal therapy in a Caucasian population. Material and Methods Sixty-eight patients with chronic periodontal disease were grouped according to their genotype: IL-6, IL-10, IL-6 and IL-10 susceptible (SCP) and non-susceptible (NSCP). All individuals were clinically evaluated at the first visit, and …

0301 basic medicineMaleLongitudinal studymedicine.medical_specialtyGenotype03 medical and health sciences0302 clinical medicineInternal medicineGenotypeMedicineHumansLongitudinal StudiesAlleleInterleukin 6General DentistryGenotypingPeriodontal DiseasesOral Medicine and PathologyPolymorphism Geneticbiologybusiness.industryInterleukin-6ResearchInterleukin030206 dentistryMiddle Aged:CIENCIAS MÉDICAS [UNESCO]SurgeryInterleukin-10030104 developmental biologyTreatment OutcomeOtorhinolaryngologyInclusion and exclusion criteriaChronic DiseaseUNESCO::CIENCIAS MÉDICASbiology.proteinSurgeryFemaleGene polymorphismbusiness
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Interleukin-25 Axis Is Involved in the Pathogenesis of Human Primary and Experimental Murine Sjögren's Syndrome

2018

Objective To investigate the role of the interleukin-25 (IL-25)/IL-17 receptor B (IL-17RB) axis in experimental Sjogren's syndrome (SS) and in patients with primary SS and primary SS-associated lymphoma. Methods Expression of IL-25, IL-17RB, IL-17B, and tumor necrosis factor receptor-associated factor 6 (TRAF6) was analyzed on minor salivary gland (SG) samples from patients with primary SS and on parotid gland samples from patients with primary SS-associated B cell non-Hodgkin's lymphoma (NHL). IL-17RB expression and the frequencies of natural group 2 innate lymphoid cells (ILC2s), inflammatory ILC2s, and M2-polarized macrophages were assessed by flow cytometry in SG mononuclear cells and p…

0301 basic medicineMaleLymphomaMacrophageImmunologyPeripheral blood mononuclear cellSalivary GlandSalivary GlandsFlow cytometry03 medical and health sciencesMice0302 clinical medicineRheumatologyInterleukin 25AnimalsHumansMedicineImmunology and AllergyLymphocytesB cellAgedReceptors Interleukin-17medicine.diagnostic_testbusiness.industryAnimalMacrophagesInnate lymphoid cellInterleukin-17Middle Agedmedicine.diseaseImmunity InnateLymphomaSettore MED/16 - Reumatologia030104 developmental biologymedicine.anatomical_structureSjogren's SyndromeImmunologyImmunology and Allergy; Rheumatology; ImmunologyLeukocytes MononuclearRituximabTumor necrosis factor alphaFemaleLymphocytebusiness030215 immunologymedicine.drugHuman
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Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction

2021

AbstractWhereas large-scale statistical analyses can robustly identify disease-gene relationships, they do not accurately capture genotype-phenotype correlations or disease mechanisms. We use multiple lines of independent evidence to show that different variant types in a single gene,SATB1, cause clinically overlapping but distinct neurodevelopmental disorders. Clinical evaluation of 42 individuals carryingSATB1variants identified overt genotype-phenotype relationships, associated with different pathophysiological mechanisms, established by functional assays. Missense variants in the CUT1 and CUT2 DNA-binding domains result in stronger chromatin binding, increased transcriptional repression…

0301 basic medicineMaleModels MolecularMISSENSE MUTATIONSCHROMATINTranscription GeneticCellMedizinDiseaseHaploinsufficiencymedicine.disease_cause0302 clinical medicineMissense mutationde novo variantsGenetics (clinical)INTERLEUKIN-2seizuresGenetics0303 health sciencesMutationChromatin bindingneurodevelopmental disordersMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]SATB1Phenotypemedicine.anatomical_structureintellectual disabilityFemaleHaploinsufficiencyteeth abnormalitiesProtein BindingNeuroinformaticsEXPRESSIONGENESMutation MissenseBiologyBINDING PROTEINREGION03 medical and health sciencesSATB1Protein DomainsReportGeneticsmedicineHPO-based analysisHumansGenetic Association StudiesHpo-based Analysis ; Satb1 ; Cell-based Functional Assays ; De Novo Variants ; Intellectual Disability ; Neurodevelopmental Disorders ; Seizures ; Teeth Abnormalities030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Matrix Attachment Region Binding Proteins030104 developmental biologyNeurodevelopmental DisordersMutationNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]030217 neurology & neurosurgerycell-based functional assays
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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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Marathon Race Affects Neutrophil Surface Molecules: Role of Inflammatory Mediators

2016

The fatigue induced by marathon races was observed in terms of inflammatory and immunological outcomes. Neutrophil survival and activation are essential for inflammation resolution and contributes directly to the pathogenesis of many infectious and inflammatory conditions. The aim of this study was to investigate the effect of marathon races on surface molecules related to neutrophil adhesion and extrinsic apoptosis pathway and its association with inflammatory markers. We evaluated 23 trained male runners at the Sao Paulo International Marathon 2013. The following components were measured: hematological and inflammatory mediators, muscle damage markers, and neutrophil function. The maratho…

0301 basic medicineMaleNeutrophilsPhysiologylcsh:MedicineApoptosisDNA fragmentationPathology and Laboratory MedicineBiochemistryNeutrophil ActivationRunningPathogenesischemistry.chemical_compoundWhite Blood CellsLeukocyte Count0302 clinical medicineAnimal CellsImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseInnate Immune SystemMultidisciplinarybiologyCell DeathInterleukinHematologyFas receptorBody FluidsNucleic acidsBloodHematocritCell ProcessesAntigens SurfaceCytokinesTumor necrosis factor alphamedicine.symptomCellular TypesAnatomyInflammation MediatorsResearch ArticleAdultCell SurvivalImmune CellseducationImmunologyInflammation03 medical and health sciencesSigns and SymptomsDiagnostic MedicineLactate dehydrogenasemedicineGeneticsHumansLeukocyte RollingHemoglobinInflammationBlood Cellsbusiness.industrylcsh:RBiology and Life SciencesProteins030229 sport sciencesCell BiologyDNAMolecular DevelopmentBlood Counts030104 developmental biologychemistryApoptosisImmune SystemImmunologybiology.proteinCreatine kinaselcsh:Qbusinesshuman activitiesDevelopmental BiologyPLoS ONE
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Clinical Characteristics of Patients Carrying the Q703K Variant of the NLRP3 Gene: A 10-year Multicentric National Study

2016

Objective.The aim of our study was to analyze the clinical and functional effect of the p.Q703K (p. Q705K, c. 2107C>A) variant of the NLRP3 gene in a population of patients screened for suspected cryopyrin-associated periodic syndrome (CAPS).Methods.Since 2002, 580 patients underwent molecular analysis for NLRP3. Data on clinical presentation, response to treatment, and longterm followup were collected using a uniform questionnaire. The pattern of cytokine secretion after lipopolysaccharide stimulation from isolated monocytes was analyzed in 3 patients carrying the p.Q703K variant and 1 patient with a chronic infantile neurologic, cutaneous, articular syndrome phenotype carrying both the…

0301 basic medicineMalePathologyMonocyteGastroenterologyMonocytesInflammasome0302 clinical medicineCRYOPYRIN-ASSOCIATED PERIODIC SYNDROMEImmunology and AllergyYoung adultChildeducation.field_of_studyCRYOPYRINMiddle AgedInterleukin-1βPhenotypeArthralgiaPhenotypeChild PreschoolNational studyCytokinesFemaleHumanAdultCryopyrinmedicine.medical_specialtyAdolescentImmunologyPopulationNLR Family03 medical and health sciencesYoung AdultRheumatologyNLRP3Internal medicineNLR Family Pyrin Domain-Containing 3 ProteinmedicineHumansPreschooleducationCytokineAllele frequencyGene030203 arthritis & rheumatologybusiness.industryCryopyrin-associated periodic syndromeInfantExanthemamedicine.diseasePyrin Domain-Containing 3 ProteinCryopyrin-Associated Periodic SyndromesINTERLEUKIN-1βCryopyrin-Associated Periodic Syndrome030104 developmental biologyINFLAMMASOMEMutationCryopyrin; Cryopyrin-Associated Periodic Syndrome; Inflammasome; Interleukin-1β; NLRP3; Adolescent; Adult; Arthralgia; Child; Child Preschool; Cryopyrin-Associated Periodic Syndromes; Cytokines; Exanthema; Female; Humans; Infant; Male; Middle Aged; Monocytes; NLR Family Pyrin Domain-Containing 3 Protein; Young Adult; Mutation; PhenotypeCytokine secretionbusinessCRYOPYRIN; CRYOPYRIN-ASSOCIATED PERIODIC SYNDROME; INFLAMMASOME; INTERLEUKIN-1β; NLRP3
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