Search results for "MESH: Inflammation"

showing 8 items of 8 documents

The Inflammatory Response in Acyl-CoA Oxidase 1 Deficiency (Pseudoneonatal Adrenoleukodystrophy)

2012

Among several peroxisomal neurodegenerative disorders, the pseudoneonatal adrenoleukodystrophy (P-NALD) is characterized by the acyl-coenzyme A oxidase 1 (ACOX1) deficiency, which leads to the accumulation of very-long-chain fatty acids ( VLCFA) and inflammatory demyelination. However, the components of this inflammatory process in P-NALD remain elusive. In this study, we used transcriptomic profiling and PCR array analyses to explore inflammatory gene expression in patient fibroblasts. Our results show the activation of IL-1 inflammatory pathway accompanied by the increased secretion of two IL-1 target genes, IL-6 and IL-8 cytokines. Human fibroblasts exposed to very-long-chain fatty acids…

MESH: Inflammationperoxisomal disordersMESH: Osteopontinmedicine.medical_treatmentMESH : ImmunohistochemistryMESH : Transcriptomechemokine receptorsVoeding Metabolisme en Genomica0302 clinical medicineEndocrinologyMESH: Reverse Transcriptase Polymerase Chain ReactionAcyl-CoA oxidasemultiple-sclerosis lesionsMESH : OsteopontinMESH : Fatty AcidsCells CulturedOligonucleotide Array Sequence Analysis[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism0303 health sciencesOxidase testMESH : Gene Expression RegulationReverse Transcriptase Polymerase Chain ReactionFatty AcidsMESH: Acyl-CoA OxidaseMESH : Reverse Transcriptase Polymerase Chain ReactionPeroxisome[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismImmunohistochemistryMESH: Gene Expression RegulationMetabolism and Genomics3. Good healthMESH: Fatty AcidsMESH : Oligonucleotide Array Sequence AnalysisCytokineMetabolisme en GenomicaACOX1AdrenoleukodystrophyNutrition Metabolism and GenomicsMESH : Acyl-CoA Oxidasemedicine.symptomInflammation MediatorsMESH: Cells Culturedmedicine.medical_specialtyMESH : Interleukin-8MESH : Interleukin-6MESH: Inflammation MediatorsInflammationBiologyin-vitroMESH : Interleukin-1MESH : Inflammation Mediators03 medical and health sciencesVoedingInternal medicinePeroxisomal disordernf-kappa-bMESH : Cells CulturedMESH : Fibroblastsmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologygene[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyNutrition030304 developmental biologyVLAGInflammationMESH: HumansMESH : InflammationInterleukin-6MESH: TranscriptomeInterleukin-8MESH : HumansMESH: Interleukin-1MESH: ImmunohistochemistryFibroblastsmedicine.diseaseMESH: Interleukin-6MESH: Interleukin-8EndocrinologyGene Expression RegulationMESH: FibroblastsMESH: Oligonucleotide Array Sequence AnalysiscellsBrief ReportsOsteopontinmicroarray analysisAcyl-CoA OxidaseTranscriptomeinterleukin-1030217 neurology & neurosurgeryx-linked adrenoleukodystrophyInterleukin-1
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Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis

2014

International audience; Adipose tissue fibrosis development blocks adipocyte hypertrophy and favors ectopic lipid accumulation. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in humans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte metabolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a functional Toll-like receptor 4 on adipose tissue hematopoietic cells is necessary for the initiation of adipose tissue fibros…

LipopolysaccharidesMESH: Signal TransductionMESH: InflammationMESH : Toll-Like Receptor 4Adipose tissueMESH : AdipocytesMESH : LipopolysaccharidesMicechemistry.chemical_compoundFibrosisAdipocyteAdipocytes[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: ObesityMESH: Animalslcsh:QH301-705.5Mice Inbred C3HToll-like receptorMESH : Diet High-FatMESH: Toll-Like Receptor 43. Good healthMESH: Insulin ResistanceAdipose TissueMESH: FibrosisMESH : Fibrosis[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : ObesityMESH : Insulin ResistanceMESH: Adipose TissueSignal Transductionmedicine.medical_specialty[SDV.IMM] Life Sciences [q-bio]/ImmunologyAdipose tissue macrophagesBiologyDiet High-FatMESH : Adipose TissueGeneral Biochemistry Genetics and Molecular BiologyImmune systemMESH : Mice Inbred C3HInternal medicineMESH : MicemedicineAnimalsHumansObesityMESH: Mice Inbred C3HMESH: MiceMESH: AdipocytesInflammationMESH : Signal TransductionMESH : InflammationMESH: HumansMESH : EndotoxemiaMESH : Humans3T3-L1medicine.diseaseFibrosisMESH : Disease Models AnimalEndotoxemiaToll-Like Receptor 4Disease Models AnimalMESH: Diet High-FatEndocrinologylcsh:Biology (General)chemistryMESH: EndotoxemiaMESH : AnimalsInsulin ResistanceMESH: Disease Models AnimalMESH: LipopolysaccharidesAdipocyte hypertrophyCell Reports
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Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
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Bimodal Recovery Pattern in Human Skeletal Muscle Induced by Exhaustive Stretch-Shortening Cycle Exercise:

2007

Introduction/Purpose: Recovery of force and stretch reflex from exhaustive stretch-shortening cycle (SSC) exercise is usually bimodal, characterized as immediate exercise-induced performance reduction, with its quick recovery followed by a longer-lasting reduction in performance. A clear parallel exists between the respective changes in performance, neural activation, and metabolic or structural exercise-induced changes. This implies the existence of potential coupling between muscle failure and the induced neural adjustments that take place along its recovery. The present study was designed to explore the evidence of this coupling more thoroughly. Methods: H- and stretch reflexes were meas…

MESH: InflammationAdultMaleReflex Stretchmedicine.medical_specialty[SDV.MHEP.PHY] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]Physical Therapy Sports Therapy and RehabilitationInflammationSubstance PPhysical exerciseIsometric exerciseMESH: Bicycling03 medical and health scienceschemistry.chemical_compound0302 clinical medicineMESH: Muscle Stretching ExercisesInternal medicineMuscle Stretching Exercisesmedicine[SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumansOrthopedics and Sports MedicineMESH: Reflex Stretch[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Stretch reflexProstaglandin E2Muscle SkeletalExerciseComputingMilieux_MISCELLANEOUSInflammationMESH: Muscle SkeletalMESH: HumansChemistrySkeletal muscleMESH: Adult030229 sport sciencesAnatomyMESH: MaleBicyclingmedicine.anatomical_structureEndocrinologyMESH: Muscle FatigueMESH: ExerciseMuscle FatigueReflex[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]medicine.symptom030217 neurology & neurosurgerymedicine.drug
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Long-term moderate magnesium-deficient diet shows relationships between blood pressure, inflammation and oxidant stress defense in aging rats

2006

International audience; Epidemiological and experimental studies have indicated a relationship among aging, dietary Mg, inflammatory stress, and cardiovascular disease. Our aim in the present study was to investigate possible links between dietary Mg, oxidant stress parameters, and inflammatory status with aging in rats. We designed a long-term study in which rats were fed for 22 months with moderately deficient (150 mg/kg), standard (800 mg/kg), or supplemented (3200 mg/kg) Mg diets. Comparisons were made with young rats fed with the same diets for 1 month. Compared to the standard and supplemented diets, the Mg-deficient diet significantly increased blood pressure, plasma interleukin-6, f…

MaleMESH: Inflammationmedicine.medical_specialtyMESH: RatsThiobarbituric acid[SDV]Life Sciences [q-bio]Blood PressureInflammationMESH: Rats Sprague-Dawley030204 cardiovascular system & hematologymedicine.disease_causeFibrinogenBiochemistryRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)Internal medicinemedicineTBARSAnimalsMESH: Animals030304 developmental biologyInflammation2. Zero hunger0303 health sciencesMESH: Oxidative StressMESH: Blood Pressuremedicine.diseaseMESH: MaleHemolysisRats3. Good healthOxidative StressLysophosphatidylcholineBlood pressureEndocrinologychemistryImmunologymedicine.symptomMagnesium DeficiencyMESH: Magnesium DeficiencyOxidative stressmedicine.drugFree Radical Biology and Medicine
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Grape seed and skin extract reduces pancreas lipotoxicity, oxidative stress and inflammation in high fat diet fed rats.

2016

IF 2.326; International audience; Obesity is related to an elevated risk of diabetes and the mechanisms whereby fat adversely affects the pancreas are poorly understood. We studied the effect of a high fat diet (HFD) on pancreas steatosis, oxidative stress and inflammation as well as the putative protection afforded by grape seed and skin extract (GSSE). HFD induced body weight gain, without affecting insulinemia, nor glycemia and dropped adiponectemia. HFD also provoked the ectopic deposition of cholesterol and triglyceride, and an oxidative stress characterized by increased lipoperoxidation and carbonylation, inhibition of antioxidant enzyme activities such as CAT, GPx and SOD, depletion …

MaleMESH : Oxidative Stress0301 basic medicineMESH: InflammationAntioxidantmedicine.medical_treatmentMESH: Grape Seed Extractmedicine.disease_causeAntioxidantschemistry.chemical_compound0302 clinical medicineMESH: ObesityVitisMESH: AnimalsMESH : Pancreas2. Zero hungerMESH: Oxidative StressMESH : Grape Seed ExtractMESH : RatsMESH : Diet High-Fatfood and beveragesGeneral MedicineMESH: Pancreas3. Good healthLipotoxicity030220 oncology & carcinogenesisSeedsMESH : AntioxidantsMESH : Obesitymedicine.symptommedicine.medical_specialtyGrape seed and skin extractMESH: RatsMESH : MaleInflammationBiologyDiet High-FatMESH : Rats WistarMESH: VitisMESH : Vitis03 medical and health sciencesDiabetes mellitusInternal medicinemedicineAnimalsObesityRats WistarPancreasPharmacologyInflammationMESH : InflammationGrape Seed ExtractTriglycerideCholesterolMESH: Antioxidants[ SDV.SP.PHARMA ] Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyMESH: Rats Wistarmedicine.diseaseMESH : SeedsMESH: MaleRatsMESH: Diet High-Fat030104 developmental biologyEndocrinologychemistryMESH: SeedsOxidative stress[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyMESH : AnimalsSteatosisOxidative stress
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Anti-inflammatory Lactobacillus rhamnosus CNCM I-3690 strain protects against oxidative stress and increases lifespan in Caenorhabditis elegans.

2012

International audience; Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabdit…

MESH: Signal TransductionMESH: InflammationAgingAnatomy and PhysiologyAntioxidantMouseNon-Clinical MedicineApplied Microbiologymedicine.medical_treatment[SDV]Life Sciences [q-bio]MESH: HT29 Cellslcsh:Medicinemedicine.disease_causelaw.inventionMiceProbiotic0302 clinical medicinelawLactobacillusMESH: ColitisInsulinMESH: Animalslcsh:ScienceCaenorhabditis elegans2. Zero hunger0303 health sciencesMultidisciplinaryMESH: Oxidative StressbiologyMESH: Reactive Oxygen SpeciesForkhead Transcription FactorsAnimal ModelsMESH: Transcription FactorsMESH: Caenorhabditis elegans ProteinsColitis3. Good healthMESH: Trinitrobenzenesulfonic Acid[SDV] Life Sciences [q-bio]MESH: LongevityMedicineFemaleHT29 CellsResearch ArticleBiotechnologySignal TransductionMESH: Receptor Insulinmedicine.drug_classLongevityMESH: InsulinMicrobiologyAnti-inflammatoryMicrobiologyIndustrial Microbiology03 medical and health sciencesMESH: Gene Expression ProfilingModel OrganismsSpecies SpecificityLactobacillus rhamnosusMESH: Caenorhabditis elegansmedicineAnimalsHumansMESH: Species SpecificityCaenorhabditis elegansCaenorhabditis elegans ProteinsBiologyMESH: Mice030304 developmental biologyInflammationHealth Care PolicyMESH: HumansGene Expression ProfilingProbioticslcsh:Rbiology.organism_classificationReceptor InsulinLactobacillusOxidative StressTrinitrobenzenesulfonic AcidQuality of Lifelcsh:QPhysiological ProcessesReactive Oxygen SpeciesMESH: LactobacillusMESH: Female030217 neurology & neurosurgeryOxidative stressBacteriaMESH: ProbioticsTranscription Factors
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Smoking and FOS expression from blood leukocyte transcripts in patients with coronary artery disease.

2011

International audience; OBJECTIVE: Analysis of the leukocyte transriptome, in particular the Finkel-Biskis-Jinkins Osteosarcoma (c-Fos) gene, which has a prominent role in inflammation, provides new insights into atherosclerosis mechanisms. Although smoking is a major risk factor, the links between smoking status and coronary artery disease (CAD) remains unclear. We aimed to analyze the relationship between smoking status and c-Fos expression in circulating leukocytes of patients with CAD. METHODS: c-Fos expression was measured by RT-Q-PCR, from blood leukocytes of 239 consecutive patients after acute myocardial infarction (MI). The patients were asked about their smoking status and stratif…

MaleMESH : RNA MessengerMESH: Chi-Square DistributionMESH : LeukocytesMESH : Prospective StudiesMESH : AgedMyocardial InfarctionSmoking PreventionMESH: Risk Assessmentc-FosMESH : Coronary Angiography0302 clinical medicineMESH : Genetic MarkersProspective StudiesMESH: Coronary Artery DiseaseAged 80 and over0303 health sciencesMESH: Middle AgedGenes fosMESH: Smoking Cessation3. Good healthMESH : SmokingMESH: Myocardial InfarctionOsteosarcomaSmoking statusCardiology and Cardiovascular MedicineGenetic Markersmedicine.medical_specialtyRisk AssessmentMESH: Leukocytes03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemHumansMESH : Middle AgedRNA MessengerMESH : Coronary Artery DiseaseRisk factorMESH : Aged 80 and overAgedChi-Square DistributionMESH: HumansMESH : Chi-Square DistributionMESH : Smoking CessationMESH : Humansmedicine.diseaseMESH: Coronary AngiographyLinear ModelsMESH: FemaleBlood leukocyte transcriptomeMESH : Genes fos030204 cardiovascular system & hematologyMESH: Genetic MarkersBioinformaticsCoronary AngiographyCoronary artery diseaseMESH: Linear ModelsCoronary artery diseaseMESH: Aged 80 and overRisk FactorsMESH: Risk FactorsMESH : Linear ModelsLeukocytesMESH : FemaleMESH : Risk AssessmentMESH: Agedc-FosbiologySmoking[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemMiddle AgedMESH : Risk Factors[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemCardiologyFemaleFrancemedicine.symptomInflammation MediatorsMESH: SmokingMESH : MaleMESH: Inflammation MediatorsInflammationMESH: Genes fosMESH: Multivariate AnalysisMESH : Inflammation MediatorsInternal medicinemedicineIn patientMESH : France030304 developmental biologyMESH: RNA Messengerbusiness.industryMESH : Multivariate AnalysisMESH: MaleMESH: Prospective StudiesMESH: FranceMultivariate Analysisbiology.proteinSmoking CessationMESH : Myocardial Infarctionbusiness
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