Search results for "interleukin-1beta"

showing 10 items of 114 documents

Influence of HMB Supplementation and Resistance Training on Cytokine Response to Resistance Exercise

2014

The purpose of this study was to determine the effects of a multinutritional supplement including amino acids, β-hydroxy-β-methylbutyrate (HMB), and carbohydrates on cytokine responses to resistance exercise and training.Seventeen healthy, college-aged men were randomly assigned to a Muscle Armor™ (MA; Abbott Nutrition, Columbus, OH) or placebo supplement group and 12 weeks of resistance training. An acute resistance exercise protocol was administered at 0, 6, and 12 weeks of training. Venous blood samples at pre-, immediately post-, and 30-minutes postexercise were analyzed via bead multiplex immunoassay for 17 cytokines.After 12 weeks of training, the MA group exhibited decreased interfer…

Malemedicine.medical_specialtyStrength trainingmedicine.medical_treatmentInterleukin-1betaMedicine (miscellaneous)Immune functionGranulocytePlaceboBody Mass IndexInterferon-gammaYoung AdultDouble-Blind MethodMuscle damageInternal medicineMyokineMyokinemedicineDietary CarbohydratesValeratesHumansMicronutrientsAmino Acidsta315Chemokine CCL4Immune function; Muscle damage; Myokine; Nutrition; Strength trainingChemokine CCL2NutritionNutrition and DieteticsInterleukin-13business.industryInterleukin-6MonocyteBody WeightInterleukin-8InterleukinResistance TrainingVenous bloodHealthy VolunteersInterleukin-10Cytokinemedicine.anatomical_structureEndocrinologyNutrition AssessmentImmunologyDietary SupplementsCytokinesStrength trainingbusiness
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The CO-releasing molecule CORM-2 is a novel regulator of the inflammatory process in osteoarthritic chondrocytes

2008

Previous work has shown that the CO-releasing molecule CORM-2 protects against cartilage degradation. The aim of this study was to examine whether CORM-2 can control the production of inflammatory mediators in osteoarthritic chondrocytes and determine the mechanisms involved.Primary cultures of chondrocytes from OA patients were stimulated with IL-1beta. The production of reactive oxygen species, nitrite, PGE(2), TNF-alpha and IL-1 receptor antagonist (IL-1Ra) were measured in the presence or absence of CORM-2. The expression of nitric oxide synthase-2 (NOS-2), cyclo-oxygenase-2 (COX-2) and microsomal PG E synthase-1 (mPGES-1) was followed by western blot and real-time PCR. Activation of nu…

Malemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IINitric Oxidemedicine.disease_causeDinoprostoneChondrocyteNitric oxidechemistry.chemical_compoundChondrocytesRheumatologyWestern blotInternal medicineOsteoarthritisOrganometallic CompoundsmedicineHumansPharmacology (medical)Cells CulturedAgedProstaglandin-E SynthasesAged 80 and overchemistry.chemical_classificationReactive oxygen speciesDose-Response Relationship Drugmedicine.diagnostic_testTumor Necrosis Factor-alphabusiness.industryNF-kappa BHypoxia-Inducible Factor 1 alpha SubunitReceptor antagonistMolecular biologyIntramolecular OxidoreductasesInterleukin 1 Receptor Antagonist ProteinEndocrinologymedicine.anatomical_structureCytokinechemistryCyclooxygenase 2PhosphorylationFemaleReactive Oxygen SpeciesbusinessOxidative stressRheumatology
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Langerin+ DCs regulate innate IL-17 production in the oral mucosa during Candida albicans-mediated infection

2018

The opportunistic fungal pathogen Candida albicans frequently causes diseases such as oropharyngeal candidiasis (OPC) in immunocompromised individuals. Although it is well appreciated that the cytokine IL-17 is crucial for protective immunity against OPC, the cellular source and the regulation of this cytokine during infection are still a matter of debate. Here, we directly visualized IL-17 production in the tongue of experimentally infected mice, thereby demonstrating that this key cytokine is expressed by three complementary subsets of CD90+ leukocytes: RAG-dependent αβ and γδ T cells, as well as RAG-independent ILCs. To determine the regulation of IL-17 production at the onset of OPC, we…

Malemedicine.medical_treatment2405 ParasitologyPathology and Laboratory Medicine10263 Institute of Experimental ImmunologyMonocytesMice0302 clinical medicineAnimal CellsCandida albicansBiology (General)Candida albicansMononuclear Phagocyte SystemFungal PathogensInnate Immune Systemeducation.field_of_studyEukaryotaMononuclear phagocyte systemFlow CytometryCorpus albicans3. Good healthSpectrophotometryMedical MicrobiologyCytokinesCytophotometryCellular Types10244 Institute of VirologyQH301-705.5Immune CellsImmunologyMicrobiology03 medical and health sciences1311 GeneticsGenetics1312 Molecular BiologyeducationMicrobial PathogensMolecular BiologyMouth2403 ImmunologyBlood CellsOrganismsBiology and Life SciencesDendritic CellsMolecular DevelopmentYeastMice Inbred C57BLMannose-Binding Lectins030104 developmental biologyImmunologyThy-1 Antigens570 Life sciences; biologyParasitologyImmunologic diseases. AllergyDigestive SystemDevelopmental Biology0301 basic medicineNeutrophilsPhysiologyInterleukin-1betaYeast and Fungal ModelsInterleukin-23White Blood CellsSpectrum Analysis TechniquesCandidiasis OralImmune PhysiologyLeukocytesMedicine and Health SciencesCandidaStainingbiologyInterleukin-172404 MicrobiologyCell StainingSpecific Pathogen-Free OrganismsInfectious DiseasesCytokineExperimental Organism SystemsAntigens SurfaceFemaleAnatomyPathogensResearch ArticleLangerinPopulationMycologyOpportunistic InfectionsResearch and Analysis MethodsTongueImmunityVirologymedicineAnimalsLectins C-TypeInterleukin 6Interleukin-6Mouth MucosaFungiCell BiologyRC581-607biology.organism_classificationSpecimen Preparation and TreatmentImmune Systembiology.protein2406 VirologySpleen030215 immunology
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Monocytes from patients with rheumatoid arthritis and type 2 diabetes mellitus display an increased production of interleukin (IL)-1β via the nucleot…

2015

Summary A better understanding about the mechanisms involved in the pathogenesis of type 2 diabetes mellitus (T2D) showed that inflammatory cytokines such as tumour necrosis factor (TNF) and interleukin (IL)-1β play a pivotal role, mirroring data largely reported in rheumatoid arthritis (RA). IL-1β is produced mainly by monocytes (MO), and hyperglycaemia may be able to modulate, in the cytoplasm of these cells, the assembly of a nucleotide-binding domain and leucine-rich repeat containing family pyrin (NLRP3)-inflammosome, a cytosolic multi-protein platform where the inactive pro-IL-1β is cleaved into active form, via caspase-1 activity. In this paper, we evaluated the production of IL-1 β …

Maletype 2 diabetes mellituInflammasomesMessengerIL-1β; NLRP3-inflammasome; rheumatoid arthritis; type 2 diabetes mellitus; Adult; Arthritis Rheumatoid; Carrier Proteins; Caspase 1; Cells Cultured; Diabetes Mellitus Type 2; Enzyme Activation; Female; Glucose; Humans; Hyperglycemia; Inflammasomes; Inflammation; Interleukin-1beta; Leukocytes Mononuclear; Male; Middle Aged; RNA Messenger; Tumor Necrosis Factor-alphaInterleukin-1betaArthritisPyrin domainInflammasomeArthritis RheumatoidRheumatoidImmunology and AllergyCells CulturedCulturedCaspase 1InterleukinDiabetes MellituMiddle AgedIL-1βTumor necrosis factor alphaNLRP3-inflammasomeFemalemedicine.symptomType 2ArthritiHumanAdultmedicine.medical_specialtyMononuclearImmunologyCaspase 1InflammationProinflammatory cytokineInternal medicineNLR Family Pyrin Domain-Containing 3 ProteinmedicineHumansRNA MessengerInflammationbusiness.industryTumor Necrosis Factor-alphaType 2 Diabetes MellitusOriginal Articlesrheumatoid arthritiLeukocytemedicine.diseaseEnzyme ActivationEndocrinologyGlucoseDiabetes Mellitus Type 2HyperglycemiaImmunologyLeukocytes MononuclearRNACellbusinessCarrier ProteinsCarrier Protein
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Cutting Edge: IL-1α Is a Crucial Danger Signal Triggering Acute Myocardial Inflammation during Myocardial Infarction

2016

Abstract Myocardial infarction (MI) induces a sterile inflammatory response that contributes to adverse cardiac remodeling. The initiating mechanisms of this response remain incompletely defined. We found that necrotic cardiomyocytes released a heat-labile proinflammatory signal activating MAPKs and NF-κB in cardiac fibroblasts, with secondary production of cytokines. This response was abolished in Myd88−/− fibroblasts but was unaffected in nlrp3-deficient fibroblasts. Despite MyD88 dependency, the response was TLR independent, as explored in TLR reporter cells, pointing to a contribution of the IL-1 pathway. Indeed, necrotic cardiomyocytes released IL-1α, but not IL-1β, and the immune acti…

MyocarditisImmunologyInterleukin-1betaMyocardial InfarctionInflammation030204 cardiovascular system & hematologyArticleProinflammatory cytokine03 medical and health sciencesMice0302 clinical medicineImmune system[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemIn vivoInterleukin-1alphamedicineImmunology and AllergyAnimalsMyocytes CardiacMyocardial infarction030304 developmental biologyInflammationMice Knockout0303 health sciencesbusiness.industryToll-Like Receptorsmedicine.disease[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemMyocarditisIL1AImmunologyMyeloid Differentiation Factor 88Cancer researchmedicine.symptomSignal transductionbusinessSignal Transduction
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Association between the interleukin-1beta polymorphisms and Alzheimer's disease: a systematic review and meta-analysis.

2008

Abstract The pro-inflammatory cytokine interleukin(IL)-1β is a main component in inflammatory pathways and is overexpressed in the brain of Alzheimer's disease (AD) patients. Several studies report associations between IL-1β polymorphisms and AD, but findings from different studies are controversial. Our aim was to verify the correlation between the single nucleotide polymorphisms (SNPs) of the IL-1β, at sites − 511 and + 3953, and AD by meta-analysis. Computerized bibliographic searches of PUBMED and AlzGene database ( http://www.alzgene.org ) were supplemented with manual searches of reference lists. There is evidence for association between IL-1β + 3953 SNP and AD, with an OR = 1.60 (95%…

OncologyDatabases Factual statistics /&/ numerical datamedicine.medical_specialtyDatabases FactualAlzheimer's disease IL-1β −511 IL-1β +3953 Polymorphism Meta-analysisPopulationInterleukin-1betaSingle-nucleotide polymorphismSubgroup analysisAlzheimer Disease geneticsMeta-Analysis as TopicPolymorphism (computer science)Alzheimer DiseaseInternal medicineGenotypemedicineSNPHumanseducationSettore MED/04 - Patologia Generaleeducation.field_of_studyPolymorphism Geneticbusiness.industryGeneral NeuroscienceComputational Biologymedicine.diseaseMeta-analysisImmunologyNeurology (clinical)Alzheimer's diseasebusinessInterleukin-1beta genetics
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Increased TNF-alfa, IL-6 and decreased IL-1beta immunohistochemical expression by the stromal spindle-shaped cells in the central giant cell granulom…

2010

Objectives: the exp ress ion of the osteoclastogenic cytokines TNF-α, IL-6 and IL-1β were immunohistochemically evaluated in periph eral (PGCG) and central (CGCG) giant cell granulomas of the jaws in order to determine diff erences between these two lesions and between the two distinct tumor cell populations (multinucleated giant cells, MGCs and stromal sp indle-sh aped cells). Study Design: Paraffin-embedd ed tiss ue sections from 40 PGCG and 40 CGCG were immunohistochemically stained using antibodies against TNF-α, IL-6 and IL-1β. The percentage of positively stained cells and the staining intensity were ass ess ed to provide a combined immunoreactivity score value. Results: TNF-α, IL-6 a…

Pathologymedicine.medical_specialtyStromal cellInterleukin-1betaProinflammatory cytokineGranuloma Giant CellOsteoclastmedicineHumansProgenitor cellGeneral DentistryOral Medicine and PathologyInterleukin-6Tumor Necrosis Factor-alphaChemistry:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseImmunohistochemistrymedicine.anatomical_structureOtorhinolaryngologyGiant cellUNESCO::CIENCIAS MÉDICASImmunohistochemistryResearch-ArticleSurgeryTumor necrosis factor alphaStromal CellsCentral giant-cell granulomaMedicina Oral Patología Oral y Cirugia Bucal
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Cellular Models and Assays to Study NLRP3 Inflammasome Biology

2020

The NLRP3 inflammasome is a multi-protein complex that initiates innate immunity responses when exposed to a wide range of stimuli, including pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). Inflammasome activation leads to the release of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 and to pyroptotic cell death. Over-activation of NLRP3 inflammasome has been associated with several chronic inflammatory diseases. A deep knowledge of NLRP3 inflammasome biology is required to better exploit its potential as therapeutic target and for the development of new selective drugs. To this purpose, in the past few years, several tools have…

Programmed cell death2019-20 coronavirus outbreakInflammasomesInterleukin-1betaReviewBiologyBiochemical assaysModels BiologicalCatalysisInflammasomelcsh:ChemistryInorganic ChemistryNLRP3NLR Family Pyrin Domain-Containing 3 ProteinPyroptosismedicineDeep knowledgeAlarminsAnimalsHumansPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyInnate immune systemintegumentary systemCell modelsPathogen-Associated Molecular Pattern MoleculesOrganic ChemistryInterleukin-18InterleukinInflammasomeGeneral MedicineBiophysical assaysImmunity InnateComputer Science ApplicationsCell biologyNLRP3 inhibitorslcsh:Biology (General)lcsh:QD1-999Mechanism of actionRead-outsmedicine.symptomInflammasome complexSignal Transductionmedicine.drugInternational Journal of Molecular Sciences
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Interferons increase cell resistance to Staphylococcal alpha-toxin.

2007

ABSTRACTMany bacterial pathogens, includingStaphylococcus aureus, use a variety of pore-forming toxins as important virulence factors. Staphylococcal alpha-toxin, a prototype β-barrel pore-forming toxin, triggers the release of proinflammatory mediators and induces primarily necrotic death in susceptible cells. However, whether host factors released in response to staphylococcal infections may increase cell resistance to alpha-toxin is not known. Here we show that prior exposure to interferons (IFNs) prevents alpha-toxin-induced membrane permeabilization, the depletion of ATP, and cell death. Moreover, pretreatment with IFN-α decreases alpha-toxin-induced secretion of interleukin 1β (IL-1β)…

Programmed cell deathStaphylococcus aureusCell Membrane Permeabilitymedicine.medical_treatmentImmunologyBacterial ToxinsInterleukin-1betaBiologyStaphylococcal infectionsMicrobiologyProinflammatory cytokineMicrobiologyCell LineHemolysin ProteinsAdenosine TriphosphateInterferonmedicineHumansSecretionCell DeathKinaseEpithelial CellsBacterial Infectionsmedicine.diseaseInfectious DiseasesCytokineProtein BiosynthesisParasitologyTumor necrosis factor alphaInterferonsFatty Acid Synthasesmedicine.drugInfection and immunity
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Proteomic Profiling of Secreted Proteins for the Hematopoietic Support of Interleukin-Stimulated Human Umbilical Vein Endothelial Cells

2013

Human umbilical cord vein endothelial cells (HUVECs) secrete a number of factors that greatly impact the proliferation and differentiation of hematopoietic stem and progenitor cells (HSPCs). These factors remain largely unknown. Here, we report on the most comprehensive proteomic profiling of the HUVEC secretome and identified 827 different secreted proteins. Two hundred and thirty-one proteins were found in all conditions, whereas 369 proteins were identified only under proinflammatory conditions following IL-1β, IL-3, and IL-6 stimulation. Thirteen proteins including complement factor b (CFb) were identified only under IL-1β and IL-3 conditions and may potentially represent HSPC prolifer…

ProteomicsSpectrometry Mass Electrospray IonizationInterleukin-1betaBiomedical EngineeringComplement C5blcsh:MedicineAntigens CD34BiologyComplement factor BUmbilical veinProinflammatory cytokineHuman Umbilical Vein Endothelial CellsHumansProgenitor cellCell ProliferationTransplantationInterleukin-6lcsh:RAntibodies MonoclonalComputational BiologyInterleukinComplement System ProteinsCell BiologyFlow CytometryHematopoietic Stem CellsMolecular biologyUp-RegulationComplement systemHaematopoiesisElectrophoresis Polyacrylamide GelInterleukin-3Stem cellPeptidesCell Transplantation
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