Search results for "NBR"

showing 10 items of 2710 documents

Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice

2017

Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer’s disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ and enhancing cognition in mice but failed totally in human. One model-dependent factor has so far been almost completely neglected: the endogenous expression of mouse APP and its effects on the transgenic models and the readout for therapeutic approaches. Here, we report that hAPP-transgenic models of …

0301 basic medicineGenetically modified mouseMaleMurine amyloid-betaBACE1-ASMice TransgenicPlaque Amyloidlcsh:RC346-429Pathology and Forensic Medicine03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein Precursor0302 clinical medicineMeningesAmyloid precursor proteinMedicineAnimalsHumansTransgenic miceSenile plaqueslcsh:Neurology. Diseases of the nervous systemNeuronsAmyloid beta-Peptidesbiologybusiness.industryAmyloidosisResearchP3 peptideBrainAmyloidosismedicine.diseasePeptide FragmentsBiochemistry of Alzheimer's diseaseAstrogliosisCell biologyMice Inbred C57BL030104 developmental biologyCaspasesAmyloid precursor proteinMutationbiology.proteinAbetaFemaleNeurology (clinical)businessNeuroscienceAlzheimer’s disease030217 neurology & neurosurgery
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Cytoskeletal transgelin 2 contributes to gender-dependent adipose tissue expandability and immune function

2019

During adipogenesis, preadipocytes' cytoskeleton reorganizes in parallel with lipid accumulation. Failure to do so may impact the ability of adipose tissue (AT) to shift between lipid storage and mobilization. Here, we identify cytoskeletal transgelin 2 (TAGLN2) as a protein expressed in AT and associated with obesity and inflammation, being normalized upon weight loss. TAGLN2 was primarily found in the adipose stromovascular cell fraction, but inflammation, TGF-β, and estradiol also prompted increased expression in human adipocytes. Tagln2 knockdown revealed a key functional role, being required for proliferation and differentiation of fat cells, whereas transgenic mice overexpressing Tagl…

0301 basic medicineGenetically modified mouseMalemedicine.medical_specialtyTHP-1 CellsBlotting WesternAdipose tissueMuscle ProteinsInflammationMice TransgenicDiet High-FatBiochemistry03 medical and health sciencesMice0302 clinical medicineImmune systemSex FactorsInternal medicineGeneticsmedicineAdipocytesAnimalsHumansObesityadipocyte protein 2CytoskeletonMolecular BiologyCytoskeletonInflammationbiologyMicrofilament ProteinsPhenotypeImmunohistochemistryMice Inbred C57BL030104 developmental biologyEndocrinologyAdipose TissueAdipogenesisbiology.proteinFemalemedicine.symptom030217 neurology & neurosurgeryBiotechnology
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DNA Damage Signaling Instructs Polyploid Macrophage Fate in Granulomas.

2018

Granulomas are immune cell aggregates formed in response to persistent inflammatory stimuli. Granuloma macrophage subsets are diverse and carry varying copy numbers of their genomic information. The molecular programs that control the differentiation of such macrophage populations in response to a chronic stimulus, though critical for disease outcome, have not been defined. Here, we delineate a macrophage differentiation pathway by which a persistent Toll-like receptor (TLR) 2 signal instructs polyploid macrophage fate by inducing replication stress and activating the DNA damage response. Polyploid granuloma-resident macrophages formed via modified cell divisions and mitotic defects and not…

0301 basic medicineGenome instabilityDNA damageLipoproteinsCellMitosisInflammationAtaxia Telangiectasia Mutated ProteinsBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicemedicineAnimalsHumansMacrophage Differentiation PathwayMitosisCell ProliferationInflammationGranulomaMacrophagesCell DifferentiationMycobacterium tuberculosisToll-Like Receptor 2Cell biologyMice Inbred C57BLTLR2030104 developmental biologymedicine.anatomical_structureImmunologymedicine.symptomCarcinogenesisDNA DamageCell
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Frailty Quantified by the "Valencia Score" as a Potential Predictor of Lifespan in Mice.

2017

The development of frailty scores suitable for mice and which resemble those used in the clinical scenario is of great importance to understand human frailty. The aim of the study was to determine an individual frailty score for each mouse at different ages and analyze the association between the frailty score and its lifespan. For this purpose, the "Valencia Score" for frailty was used. Thus, a longitudinal study in mice was performed analyzing weight loss, running time and speed, grip strength and motor coordination at the late-adult, mature and old ages (40, 56 and 80 weeks old, respectively). These parameters are equivalent to unintentional weight loss, poor endurance, slowness, weaknes…

0301 basic medicineGerontologyWeaknessLongitudinal studyAgingFrail ElderlyLongevityHealthy Aging03 medical and health sciencesGrip strengthMice0302 clinical medicineWeight lossWeight LossmedicineAnimalsHumansLongitudinal StudiesMaze LearningClinical scenarioGeriatric AssessmentAgedMice Inbred ICRFrailtyHand Strengthbusiness.industryLow activityAging PrematureRunning timeMotor coordination030104 developmental biologyPhenotypeModels AnimalPhysical EnduranceFemaleGeriatrics and Gerontologymedicine.symptombusiness030217 neurology & neurosurgeryThe journals of gerontology. Series A, Biological sciences and medical sciences
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A New Frailty Score for Experimental Animals Based on the Clinical Phenotype: Inactivity as a Model of Frailty.

2016

The development of animal models to study human frailty is important to test interventions to be translated to the clinical practice. The aim of this work was to develop a score for frailty in experimental animals based in the human frailty phenotype. We also tested the effect of physical inactivity in the development of frailty as determined by our score. Male C57Bl/6J mice, individually caged, were randomly assigned to one of two groups: sedentary (inactive) or spontaneous wheel-runners. We compared the sedentary versus the active lifestyle in terms of frailty by evaluating the clinical criteria used in humans: unintentional weight loss; poor endurance (running time); slowness (running sp…

0301 basic medicineGerontologymedicine.medical_specialtyWeaknessAgingFrail ElderlyPsychological interventionTranslational Research Biomedical03 medical and health sciencesGrip strengthMice0302 clinical medicinePhysical medicine and rehabilitationWeight lossPhysical Conditioning AnimalActivities of Daily LivingmedicineAnimalsHumansMobility LimitationClinical phenotypeAgedbusiness.industrymedicine.diseaseMotor coordinationRunning timeMice Inbred C57BL030104 developmental biologyResearch DesignSpainSarcopeniaModels AnimalGeriatrics and Gerontologymedicine.symptomSedentary Behaviorbusiness030217 neurology & neurosurgeryThe journals of gerontology. Series A, Biological sciences and medical sciences
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Duodenal Bacteria From Patients With Celiac Disease and Healthy Subjects Distinctly Affect Gluten Breakdown and Immunogenicity

2016

Background & Aims Partially degraded gluten peptides from cereals trigger celiac disease (CD), an autoimmune enteropathy occurring in genetically susceptible persons. Susceptibility genes are necessary but not sufficient to induce CD, and additional environmental factors related to unfavorable alterations in the microbiota have been proposed. We investigated gluten metabolism by opportunistic pathogens and commensal duodenal bacteria and characterized the capacity of the produced peptides to activate gluten-specific T-cells from CD patients. Methods We colonized germ-free C57BL/6 mice with bacteria isolated from the small intestine of CD patients or healthy controls, selected for their in v…

0301 basic medicineGlutensDuodenumTissue transglutaminaseT-Lymphocytesdigestive systemMicrobiologyMice03 medical and health sciencesLactobacillusmedicineAnimalsHumansImmunogenetic Phenomenachemistry.chemical_classificationHepatologybiologyImmunogenicityGastroenterologynutritional and metabolic diseasesmedicine.diseasebiology.organism_classificationGlutendigestive system diseasesSmall intestineAltered Schaedler floraMice Inbred C57BLCeliac DiseaseLactobacillus030104 developmental biologymedicine.anatomical_structurechemistryBacterial TranslocationCase-Control StudiesPseudomonas aeruginosaImmunologybiology.proteinGliadinDysbiosisGastroenterology
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Disentangling the effect of host genetics and gut microbiota on resistance to an intestinal parasite

2019

11 pages; International audience; Resistance to infection is a multifactorial trait, and recent work has suggested that the gut microbiota can also contribute to resistance. Here, we performed a fecal microbiota transplant to disentangle the contribution of the gut microbiota and host genetics as drivers of resistance to the intestinal nematode Heligmosomoides polygyrus. We transplanted the microbiota of a strain of mice (SJL), resistant to H. polygyrus, into a susceptible strain (CBA) and vice-versa. We predicted that if the microbiota shapes resistance to H. polygyrus, the FMT should reverse the pattern of resistance between the two host strains. The two host strains had different microbi…

0301 basic medicineHeligmosomoides polygyrusGut floramedicine.disease_causeFecal microbiota transplant0302 clinical medicinefluids and secretionsMESH: Fecal Microbiota TransplantationParasite hostingColonizationMESH: AnimalsMESH: Strongylida InfectionsDisease ResistanceGeneticsNematospiroides dubiusbiology[SDV.BA]Life Sciences [q-bio]/Animal biologyFecal Microbiota Transplantation3. Good healthInfectious DiseasesMESH: Nematospiroides dubiusGenetic Background030231 tropical medicineIntestinal parasiteHeterologousMice Inbred StrainsMESH: Disease ResistanceMESH: Host-Parasite InteractionsMESH: Mice Inbred Strainsdigestive systemMESH: Gastrointestinal MicrobiomeHost-Parasite Interactions03 medical and health sciencesImmunityparasitic diseasesmedicineAnimals[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyStrongylida InfectionsHost (biology)ImmunityLife history traitsMESH: Genetic Backgroundbiology.organism_classificationGastrointestinal MicrobiomeDisease Models Animalstomatognathic diseases030104 developmental biologyParasitologyHeligmosomoides polygyrusMESH: Disease Models Animal[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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TLR3-independent activation of mast cells by cytomegalovirus contributes to control of pulmonary infection.

2017

Interstitial pneumonia is a life-threatening clinical manifestation of human cytomegalovirus (hCMV) infection. In particular, it can be deadly in patients with hematopoietic malignancies who undergo hematopoietic cell transplantation (HCT) in whom a ‘window of risk’, which is defined by transient immunodeficiency, occurs between hematoablative therapeutic treatment and immunological reconstitution. As few clinical studies have addressed the underlying mechanisms for this phenomenon, a mouse model of HCT and murine cytomegalovirus (mCMV) infection has been established and has revealed a key role for antiviral CD8+ T cells in controlling pulmonary infections. Using this mouse model, recent st…

0301 basic medicineHuman cytomegalovirusLung DiseasesChemokineImmunologyCongenital cytomegalovirus infectionCytomegalovirusModels BiologicalCCL503 medical and health sciencesmedicineImmunology and AllergyAnimalsMast Cells030102 biochemistry & molecular biologybiologyDegranulationvirus diseasesmedicine.diseaseResearch HighlightToll-Like Receptor 3TransplantationMice Inbred C57BL030104 developmental biologyInfectious DiseasesTRIFImmunologyCytomegalovirus Infectionsbiology.proteinCD8Cellularmolecular immunology
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Clr-a: A Novel Immune-Related C-Type Lectin-like Molecule Exclusively Expressed by Mouse Gut Epithelium

2017

Abstract The mouse gut epithelium represents a constitutively challenged environment keeping intestinal commensal microbiota at bay and defending against invading enteric pathogens. The complex immunoregulatory network of the epithelial barrier surveillance also involves NK gene complex (NKC)–encoded C-type lectin-like molecules such as NKG2D and Nkrp1 receptors. To our knowledge, in this study, we report the first characterization of the orphan C-type lectin-like molecule Clr-a encoded by the Clec2e gene in the mouse NKC. Screening of a panel of mouse tissues revealed that Clec2e transcripts are restricted to the gastrointestinal tract. Using Clr-a–specific mAb, we characterize Clr-a as a …

0301 basic medicineImmunoblottingImmunologyCryptFluorescent Antibody TechniqueCell SeparationBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationC-type lectinAnimalsImmunology and AllergyLectins C-TypeIntestinal MucosaReceptorMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionFlow CytometryNKG2DIntestinal epitheliumMolecular biologyGut EpitheliumMice Inbred C57BLImmunosurveillance030104 developmental biology030215 immunologyThe Journal of Immunology
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Donor interleukin-22 and host type I interferon signaling pathway participate in intestinal graft-versus-host disease via STAT1 activation and CXCL10.

2014

Acute graft-versus-host disease (aGVHD) remains a major complication following allogeneic hematopoietic cell transplantation, limiting the success of this therapy. We previously reported that interleukin-22 (IL-22) participates to aGVHD development, but the underlying mechanisms of its contribution remain poorly understood. In this study, we analyzed the mechanism of the pathological function of IL-22 in intestinal aGVHD. Ex-vivo colon culture experiments indicated that IL-22 was able to induce Th1-like inflammation via signal transducer and activator of transcription factor-1 (STAT1) and CXCL10 induction in the presence of type I interferon (IFN). To evaluate a potential synergy between IL…

0301 basic medicineImmunologyGraft vs Host DiseaseInflammationReceptor Interferon alpha-betaInterleukin 2203 medical and health sciencesMiceInterferonimmune system diseasesBone MarrowmedicineImmunology and AllergyCXCL10AnimalsTransplantation HomologousHumansSTAT1Intestine LargeIntestinal MucosaBone Marrow TransplantationMice KnockoutMice Inbred BALB CbiologyInterleukinsTh1 CellsTissue DonorsTransplantationMice Inbred C57BLChemokine CXCL10030104 developmental biologymedicine.anatomical_structuresurgical procedures operativeSTAT1 Transcription FactorGene Expression RegulationHematologic NeoplasmsImmunologyInterferon Type Ibiology.proteinSTAT proteinBone marrowmedicine.symptomWhole-Body Irradiationmedicine.drugSignal Transduction
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