Search results for "Inflammation."

showing 10 items of 2627 documents

Cutting Edge: IL-6–Driven Immune Dysregulation Is Strictly Dependent on IL-6R α-Chain Expression

2020

Abstract IL-6 binds to the IL-6R α-chain (IL-6Rα) and signals via the signal transducer gp130. Recently, IL-6 was found to also bind to the cell surface glycoprotein CD5, which would then engage gp130 in the absence of IL-6Rα. However, the biological relevance of this alternative pathway is under debate. In this study, we developed a mouse model, in which murine IL-6 is overexpressed in a CD11c-Cre–dependent manner. Transgenic mice developed a lethal immune dysregulation syndrome with increased numbers of Ly-6G+ neutrophils and Ly-6Chi monocytes/macrophages. IL-6 overexpression promoted activation of CD4+ T cells while suppressing CD5+ B-1a cell development. However, additional ablation of …

Genetically modified mouseImmunologyInflammationMice Transgenicmedicine.disease_cause03 medical and health sciencesMice0302 clinical medicineRare DiseasesmedicineImmunology and AllergyAnimals2.1 Biological and endogenous factorsInflammatory and Immune SystemReceptorSTAT3biologyCell growthChemistryInterleukin-6Immune dysregulationGlycoprotein 130Receptors Interleukin-6Cell biologybiology.proteinAlternative complement pathwaymedicine.symptom030215 immunologySignal TransductionThe Journal of Immunology
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Treatment of allergic airway inflammation and hyperresponsiveness by antisense-induced local blockade of GATA-3 expression.

2001

Recent studies in transgenic mice have revealed that expression of a dominant negative form of the transcription factor GATA-3 in T cells can prevent T helper cell type 2 (Th2)-mediated allergic airway inflammation in mice. However, it remains unclear whether GATA-3 plays a role in the effector phase of allergic airway inflammation and whether antagonizing the expression and/or function of GATA-3 can be used for the therapy of allergic airway inflammation and hyperresponsiveness. Here, we analyzed the effects of locally antagonizing GATA-3 function in a murine model of asthma. We could suppress GATA-3 expression in interleukin (IL)-4–producing T cells in vitro and in vivo by an antisense ph…

Genetically modified mouseOvalbuminmedicine.medical_treatmentImmunologyT cellsInflammationGATA3 Transcription FactorGATA-3Proinflammatory cytokineMiceTh2 CellsImmunology and AllergyMedicineAnimalsInterleukin 9LungInterleukin 4Mice Inbred BALB Cbiologybusiness.industryInterleukin-9InterleukinOligonucleotides Antisenseasthmaantisense DNADNA-Binding ProteinsEosinophilsOvalbuminCytokineImmunologybiology.proteinTrans-ActivatorsFemaleOriginal ArticleInterleukin-4Th2 cytokinesmedicine.symptomBronchial HyperreactivitybusinessThe Journal of experimental medicine
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A key pathogenic role for the STAT1/T-bet signaling pathway in T-cell-mediated liver inflammation.

2003

TH1 cytokines have been suggested to contribute to the pathogenesis of T-cell-mediated liver injury and inflammation. However, the molecular signaling pathways involved in such injury are still poorly understood. In the present study, we investigated the role of the STAT1/T-bet signaling pathway in a murine model of T-cell-mediated liver inflammation induced by the application of concanavalin A (Con A) using newly created STAT1 transgenic mice as well as STAT1- and T-bet-deficient mice. Liver injury induced by Con A was associated with an increase of both pSTAT1 and T-bet levels in the liver. Furthermore, functional studies suggested a pathogenic role for STAT1 in Con A-induced liver injury…

Genetically modified mouseT cellTransgeneT-LymphocytesInflammationMice TransgenicBiologyHepatitisInterferon-gammaMicemedicineConcanavalin AAnimalsInterferon gammaLiver injuryHepatologymedicine.diseasePhosphoproteinsDNA-Binding ProteinsMice Inbred C57BLIRF1medicine.anatomical_structureSTAT1 Transcription FactorLiverImmunologyTrans-ActivatorsSignal transductionmedicine.symptomT-Box Domain Proteinsmedicine.drugInterferon Regulatory Factor-1Signal TransductionTranscription FactorsHepatology (Baltimore, Md.)
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Effects of neuron-specific ADAM10 modulation in an in vivo model of acute excitotoxic stress.

2008

A disintegrin and metalloprotease (ADAM) 10 is the main candidate enzyme for the alpha-secretase processing of the amyloid precursor protein (APP). Neuron-specific ADAM10 overexpression proved beneficial in the APP[V717I] mutant Alzheimer mouse model [Postina R, Schroeder A, Dewachter I, Bohl J, Schmitt U, Kojro E, Prinzen C, Endres K, Hiemke C, Blessing M, Flamez P, Dequenne A, Godaux E, van Leuven F, Fahrenholz F (2004) A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model. J Clin Invest 113:1456-1464]. Since Alzheimer patients have a high prevalence for epileptic seizures, we investigated the effects of ADAM10 modula…

Genetically modified mousemedicine.medical_specialtyIndolesADAM10TransgeneExcitotoxicityMice Transgenicmedicine.disease_causeNeuroprotectionHippocampusADAM10 ProteinAmyloid beta-Protein PrecursorMiceLeucineSeizuresStress PhysiologicalInternal medicineGlial Fibrillary Acidic ProteinmedicineAmyloid precursor proteinAnimalsNeuroinflammationNeuronsAnalysis of VarianceKainic AcidbiologyCell DeathDose-Response Relationship DrugChemistryGeneral NeuroscienceNeurodegenerationMembrane ProteinsValinemedicine.diseaseADAM ProteinsDisease Models AnimalEndocrinologyGene Expression RegulationMutationbiology.proteinAmyloid Precursor Protein SecretasesPlant LectinsNeuroscienceNeuroscience
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Naturally occurring autoantibodies interfere with β-amyloid metabolism and improve cognition in a transgenic mouse model of Alzheimer's disease 24 h …

2013

There is evidence that naturally occurring antibodies directed against Aβ (nAbs-Aβ) have a role in Aβ-metabolism and Aβ-clearance. The presence of nAbs-Aβ leads to a reduction in amyloid fibrillation and thus a reduction in their toxicity. We investigated the effects of nAbs-Aβ in respect to oligomerization and used the Tg2576 transgenic mouse model in order to investigate the rapid effect with a single-dose (24 h) on oligomer breakdown and cytokine secretion along with immunohistochemical characterization of synaptic plasticity. nAbs-Aβ were able to reduce toxic oligomer concentration with an increase in Aβ-monomers. Cytokine secretion was significantly reduced. Synaptic plasticity was als…

Genetically modified mousemedicine.medical_specialtytoxic oligomersAmyloidBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicBiologyAnimals Genetically ModifiedCellular and Molecular NeuroscienceMiceCognitionAlzheimer DiseaseInternal medicinemedicineAnimalsBiological PsychiatryAutoantibodiesAmyloid beta-Peptidesβ-amyloidbehaviorAutoantibodyAlzheimer's diseasemedicine.diseasenatural occurring autoantibodiesCell biologyPsychiatry and Mental healthDisease Models AnimalEndocrinologyinflammationSynaptic plasticityToxicitybiology.proteinCytokinesCytokine secretionOriginal ArticleFemaleAlzheimer's diseaseAntibodyTranslational Psychiatry
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Disrupting immune regulation incurs transient costs in male reproductive function.

2014

9 pages; International audience; BACKGROUND: Immune protection against pathogenic organisms has been shown to incur costs. Previous studies investigating the cost of immunity have mostly focused on the metabolic requirements of immune maintenance and activation. In addition to these metabolic costs, the immune system can induce damage to the host if the immune response is mis-targeted or over-expressed. Given its non-specific nature, an over-expressed inflammatory response is often associated with substantial damage for the host. Here, we investigated the cost of an over-expressed inflammatory response in the reproductive function of male mice. METHODOLOGY/PRINCIPAL FINDINGS: We experimenta…

Genetics and Molecular Biology (all)0106 biological sciencesMalemedicine.medical_treatmentlcsh:MedicineBiochemistry01 natural sciencesMiceMonoclonalReceptorsTestis[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/Symbiosis[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyReceptors Interleukin-10Animals; Antibodies Monoclonal; Body Weight; Inflammation; Male; Mice; Organ Size; Receptors Interleukin-10; Reproduction; Spermatozoa; Testis; Immunomodulation; Medicine (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)lcsh:ScienceReceptorImmune Response0303 health sciencesMultidisciplinaryReproductive functionMedicine (all)ReproductionAging and ImmunityAntibodies MonoclonalOrgan SizeSpermatozoaInterleukin-103. Good healthCytokineCytokines[SDV.IMM]Life Sciences [q-bio]/Immunologymedicine.symptomResearch ArticleInfertilityEvolutionary ImmunologyImmunologyInflammationBiology010603 evolutionary biologyImmune SuppressionAntibodiesImmunomodulation03 medical and health sciencesImmune systemImmunitymedicineAnimalsBiology030304 developmental biologyInflammationEvolutionary Biology[ SDE.BE ] Environmental Sciences/Biodiversity and Ecologylcsh:RBody WeightImmunityImmunoregulationmedicine.diseaseBlockadeAgricultural and Biological Sciences (all)Immune SystemImmunologyHumoral Immunitylcsh:Q[SDE.BE]Environmental Sciences/Biodiversity and Ecology[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/Symbiosis
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Effects of eight weeks of time-restricted feeding (16/8) on basal metabolism, maximal strength, body composition, inflammation, and cardiovascular ri…

2016

Background: Intermittent fasting (IF) is an increasingly popular dietary approach used for weight loss and overall health. While there is an increasing body of evidence demonstrating beneficial effects of IF on blood lipids and other health outcomes in the overweight and obese, limited data are available about the effect of IF in athletes. Thus, the present study sought to investigate the effects of a modified IF protocol (i.e. time-restricted feeding) during resistance training in healthy resistance-trained males. Methods: Thirty-four resistance-trained males were randomly assigned to time-restricted feeding (TRF) or normal diet group (ND). TRF subjects consumed 100 % of their energy needs…

Genetics and Molecular Biology (all)0301 basic medicineAdultMalemedicine.medical_specialtyCalorieTime FactorsNormal dietBody builders; Body composition; Fasting; Intermittent fasting; Resistance training; Time-restricted feeding; Medicine (all); Biochemistry Genetics and Molecular Biology (all)Blood lipidsPhysiology030209 endocrinology & metabolismIntermittent fastingOverweightBody buildersBiochemistryBody compositionGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineWeight lossRisk FactorsInternal medicineTime-restricted feedingIntermittent fastingmedicineHumansResting energy expenditureMuscle StrengthCaloric RestrictionMedicine(all)InflammationBiochemistry Genetics and Molecular Biology (all)030109 nutrition & dieteticsbusiness.industryBiochemistry Genetics and Molecular Biology(all)Medicine (all)ResearchResistance TrainingGeneral MedicineFeeding BehaviorFastingEndocrinologyCardiovascular DiseasesBasal metabolic rateBasal Metabolismmedicine.symptomBody builderbusinessJournal of translational medicine
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C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation

2015

Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here we show that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours. Compared with wild-type (WT) or C3- or C5-deficient mice, C1q-deficient (C1qa−/−) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonged survival. This effect is not attributable to differences in the tumour-infiltrating immune cells. Tumours developing in WT mice display early deposition of C1q, higher vascular density and an increase in the number of lung metastases compared with C1qa−/− mi…

Genetics and Molecular Biology (all)0301 basic medicinePROTEINGeneral Physics and AstronomyMELANOMAApoptosisInbred C57BLBiochemistryDISEASEAnimals; Apoptosis; Cell Line Tumor; Cell Movement; Cell Proliferation; Complement Activation; Complement C1q; Complement C3; Complement C5; Humans; Mice; Mice Inbred C57BL; Mice Knockout; Neoplasms; Biochemistry Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)Micefluids and secretionsCell Movementimmune system diseasesNeoplasmsIMMUNE-RESPONSEskin and connective tissue diseasesComplement ActivationComplement C1qMice KnockoutComplement component 5TumorMultidisciplinaryQChemistry (all)Complement C5Complement C33. Good healthCell biologyMultidisciplinary SciencesDEFICIENCYmedicine.anatomical_structureScience & Technology - Other TopicsHumanKnockoutSciencechemical and pharmacologic phenomenaBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyTROPHOBLAST INVASIONMECHANISMSCell LinePhysics and Astronomy (all)03 medical and health sciencesClassical complement pathwayImmune systemINFLAMMATIONCell Line TumormedicineAnimalsHumansCell ProliferationScience & TechnologyBiochemistry Genetics and Molecular Biology (all)AnimalCell growthEFFECTOR SYSTEMComplement C1qApoptosiGeneral ChemistryComplement systemMice Inbred C57BL030104 developmental biologyCancer cellNeoplasmBone marrowANTIBODY THERAPYNature Communications
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Dysbiosis and zonulin upregulation alter gut epithelial and vascular barriers in patients with ankylosing spondylitis

2017

BackgroundDysbiosis has been recently demonstrated in patients with ankylosing spondylitis (AS) but its implications in the modulation of intestinal immune responses have never been studied. The aim of this study was to investigate the role of ileal bacteria in modulating local and systemic immune responses in AS.MethodsIleal biopsies were obtained from 50 HLA-B27+ patients with AS and 20 normal subjects. Silver stain was used to visualise bacteria. Ileal expression of tight and adherens junction proteins was investigated by TaqMan real-time (RT)-PCR and immunohistochemistry. Serum levels of lipopolysaccharide (LPS), LPS-binding protein (LPS-BP), intestinal fatty acid-BP (iFABP) and zonulin…

Genetics and Molecular Biology (all)Fatty Acid-Binding ProteinAnkylosing SpondylitisMonocyteBiochemistryMonocytesTransgenic0302 clinical medicineIntestinal MucosaMembrane GlycoproteinsZonulinCadherinsAdherens JunctionUp-RegulationAntigenAcute DiseaseMembrane GlycoproteinRats TransgenicInfectionHumanAnkylosingImmunologyGeneral Biochemistry Genetics and Molecular BiologyArticlePermeabilityTight Junctions03 medical and health sciencesRheumatologyAntigens CDIleumAnti-Bacterial AgentHuman Umbilical Vein Endothelial CellsHumansRNA MessengerEndotheliumProtein PrecursorsAnkylosing SpondylitiBiochemistry Genetics and Molecular Biology (all)BacteriaAnimalmedicine.diseaseDysbiosiSettore MED/16 - Reumatologia030104 developmental biologychemistryCase-Control StudiesImmunologyRatCarrier ProteinsAcute-Phase ProteinsSpondylitis0301 basic medicineLipopolysaccharidesLipopolysaccharideMessengerAcute-Phase ProteinGene Expressionchemistry.chemical_compoundIntestinal mucosaImmunology and AllergyMembrane ProteinHLA-B27 AntigenCaco-2 CellTight junctionTight JunctionAdherens JunctionsIleitisIleitiAnti-Bacterial AgentsCDmedicine.anatomical_structureAnkylosing Spondylitis; Infections; Inflammation; Acute Disease; Acute-Phase Proteins; Adherens Junctions; Animals; Anti-Bacterial Agents; Antigens CD; Bacteria; Caco-2 Cells; Cadherins; Carrier Proteins; Case-Control Studies; Cholera Toxin; Chronic Disease; Dysbiosis; Endothelium; Fatty Acid-Binding Proteins; Gene Expression; HLA-B27 Antigen; Human Umbilical Vein Endothelial Cells; Humans; Ileitis; Ileum; Interleukin-8; Intestinal Mucosa; Junctional Adhesion Molecule A; Lipopolysaccharides; Membrane Glycoproteins; Membrane Proteins; Monocytes; Permeability; RNA Messenger; Rats; Rats Transgenic; Spondylitis Ankylosing; Tight Junctions; Up-Regulationmedicine.symptomCase-Control StudieCholera ToxinHuman Umbilical Vein Endothelial CellLipopolysaccharideInflammationInfectionsFatty Acid-Binding ProteinsAdherens junctionmedicineAnkylosing Spondylitis; Infections; Inflammation; Acute Disease; Acute-Phase Proteins; Adherens Junctions; Animals; Anti-Bacterial Agents; Antigens CD; Bacteria; Caco-2 Cells; Cadherins; Carrier Proteins; Case-Control Studies; Cholera Toxin; Chronic Disease; Dysbiosis; Endothelium; Fatty Acid-Binding Proteins; Gene Expression; HLA-B27 Antigen; Human Umbilical Vein Endothelial Cells; Humans; Ileitis; Ileum; Interleukin-8; Intestinal Mucosa; Junctional Adhesion Molecule A; Lipopolysaccharides; Membrane Glycoproteins; Membrane Proteins; Monocytes; Permeability; RNA Messenger; Rats; Rats Transgenic; Spondylitis Ankylosing; Tight Junctions; Up-Regulation; Immunology and Allergy; Rheumatology; Immunology; Biochemistry Genetics and Molecular Biology (all)AnimalsSpondylitis AnkylosingAntigensSpondyliti030203 arthritis & rheumatologyInflammationHaptoglobinsbusiness.industryMonocyteInterleukin-8Membrane ProteinsRatsJunctional Adhesion Molecule AChronic DiseaseCadherinDysbiosisRNACaco-2 CellsCarrier ProteinbusinessDysbiosis
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Interleukin-10 promoter polymorphism in sporadic Alzheimer's disease.

2003

Proinflammatory cytokines and acute-phase proteins play an important role in Alzheimer's disease (AD) neurodegeneration, and common polymorphisms of genes controlling their high production have been shown to be associated with AD. Thus, AD patients display a proinflammatory genotype and the control of inflammation might play a protective role in AD development. By sequence-specific probes, we have evaluated the role of anti-inflammatory cytokine interleukin(IL)-10 in AD, by analysing in 132 AD patients and 213 healthy controls the prevalence of three different haplotypes, involving three single-nucleotide polymorphisms (SNPs) at -1082 (G--A), -819 (C--T) and -592 (C--A) nucleotides of IL-10…

GeneticsInflammationImmunologyHaplotypeInterleukinSingle-nucleotide polymorphismBiologyProinflammatory cytokineInterleukin-10Interleukin 10Alzheimer DiseaseImmunologyGenotypeGeneticsSNPHumansAllelePromoter Regions GeneticGenetics (clinical)Genes and immunity
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