Search results for "MESH: Toll-Like Receptor 4"

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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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