Search results for "macrophage"

showing 10 items of 781 documents

Peritoneal Cavity is a Route for Gut-Derived Microbial Signals to Promote Autoimmunity in Non-Obese Diabetic Mice

2015

Macrophages play a crucial role in innate immune reactions, and peritoneal macrophages (PMs) guard the sterility of this compartment mainly against microbial threat from the gut. Type 1 diabetes (T1D) is an autoimmune disease in which gut microbiota and gut immune system appear to contribute to disease pathogenesis. We have recently reported elevated free radical production and increased permeability of gut epithelium in non-obese diabetic (NOD) mice. Impaired barrier function could lead to bacterial leakage to the peritoneal cavity. To explore the consequences of impaired gut barrier function on extra-intestinal immune regulation, we characterized peritoneal lavage cells from young newly w…

Antigens Differentiation T-LymphocyteLipopolysaccharidesmedicine.medical_specialtymiceT-LymphocytesT cellBlotting WesternImmunologyWeaningNodBiologyta3111Peritoneal cavityImmune systemSpecies SpecificityAntigens CDMice Inbred NODInternal medicinediabeticmedicineAnimalsLectins C-TypeIntestinal Mucosamicrobial signalsCells CulturedNOD miceMice Inbred BALB CInnate immune systemTumor Necrosis Factor-alphanon-obeseMicrobiotaautoimmunityta1182ta3141General MedicineFlow CytometryGut EpitheliumIntestinesMice Inbred C57BLInterleukin-1 Receptor-Associated KinasesEndocrinologymedicine.anatomical_structureperitoneal cavityImmunologyMacrophages PeritonealTumor necrosis factor alphaInjections IntraperitonealSignal TransductionScandinavian Journal of Immunology
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Oxidative stress protection by manganese complexes of tail-tied aza-scorpiand ligands.

2015

The Mn2+ coordination chemistry of double scorpiand ligands in which two polyazacyclophane macrocycles have been connected by pyridine, phenanthroline and bipyridine spacers has been studied by potentiometry, paramagnetic NMR and electrochemistry. All ligands show high stability with Mn2+ and the complexes were formed in a wide pH range. DFT calculations support the structures and coordination geometries derived from the study. A remarkable antioxidant activity was evidenced for these systems by the McCord-Fridovich assay and in Escherichiacoli sodAsodB deficient bacterial cells. The three systems were tested as anti-inflammatory drugs in human macrophages measuring the accumulation of cyto…

AntioxidantStereochemistrymedicine.medical_treatmentPhenanthrolineInorganic chemistrychemistry.chemical_elementManganese010402 general chemistryElectrochemistry01 natural sciencesBiochemistryAntioxidantsCoordination complexInorganic ChemistrySuperoxide dismutasechemistry.chemical_compoundBipyridineBacterial ProteinsCoordination ComplexesCell Line TumorPyridinemedicineEscherichia coliHumanschemistry.chemical_classificationManganesebiology010405 organic chemistryChemistrySuperoxide DismutaseMacrophagesAnti-Inflammatory Agents Non-Steroidal0104 chemical sciencesOxidative Stressbiology.proteinJournal of inorganic biochemistry
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Does unsaponifiable fraction of grape seed oil attenuate nitric oxide production, oxidant and cytotoxicity activities.

2019

Triterpenoids, tocopherols, and phytosterols presented in unsaponifiable fraction of grape seed oil have several beneficial effects comprising antioxidant, anti-inflammatory, and antitumor capacities. In this study, the unsaponifiable fraction of three Tunisian grape seed varieties (Vitis vinifera L.), namely Merlot, Carignan, and Syrah, was investigated. The identified compounds were two triterpenic compounds (β-amyrin, lanosterol), six phytosterols (campesterol, ∆7 -avenasterol, stigmasterol, β-sitosterol, β-sitostanol, cholesterol), and three tocopherols (α, β, and γ tocopherols). The unsaponifiable fraction had significant protection against oxidative damage by modulating NO production …

Antioxidantfood.ingredient030309 nutrition & dieteticsCell SurvivalCampesterolmedicine.medical_treatmentBiophysicsFraction (chemistry)AvenasterolNitric OxideGrape seed oil03 medical and health scienceschemistry.chemical_compoundMice0404 agricultural biotechnologyfoodmedicineAnimalsVitisFood sciencePharmacology0303 health sciencesStigmasterolGrape Seed ExtractMacrophagesfood and beverages04 agricultural and veterinary sciencesCell BiologyOxidants040401 food scienceRAW 264.7 CellschemistryUnsaponifiableComposition (visual arts)BiomarkersFood ScienceJournal of food biochemistry
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Inhibition of endocannabinoid-degrading enzyme fatty acid amide hydrolase increases atherosclerotic plaque vulnerability in mice

2013

The role of endocannabinoids such as anandamide during atherogenesis remains largely unknown. Fatty acid amide hydrolase (FAAH) represents the key enzyme in anandamide degradation, and its inhibition is associated with subsequent higher levels of anandamide. Here, we tested whether selective inhibition of FAAH influences the progression of atherosclerosis in mice. Selective inhibition of FAAH using URB597 resulted in significantly increased plasma levels of anandamide compared to control, as assessed by mass spectrometry experiments in mice. Apolipoprotein E-deficient (ApoE(-/-)) mice were fed a high-fat, cholesterol-rich diet to induce atherosclerotic conditions. Simultaneously, mice recei…

Apolipoprotein Emedicine.medical_specialtyApolipoprotein BNeutrophilsPolyunsaturated Alkamidesmedicine.medical_treatmentIntraperitoneal injectionGene ExpressionArachidonic AcidsDiet High-FatAmidohydrolasesMicechemistry.chemical_compoundApolipoproteins EWestern blotCell MovementSuperoxidesFatty acid amide hydrolaseInternal medicinemedicineAnimalsEnzyme InhibitorsMolecular BiologyMice Knockoutbiologymedicine.diagnostic_testChemistryMacrophagesAnandamideURB597Dietary FatsEndocannabinoid systemPlaque AtheroscleroticEndocrinologyBenzamidesbiology.proteinCarbamatesCardiology and Cardiovascular MedicineEndocannabinoidsJournal of Molecular and Cellular Cardiology
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Knock-down of the oxysterol receptor LXRα impairs cholesterol efflux in human primary macrophages: lack of compensation by LXRβ activation.

2012

Liver X Receptors (LXRs) α and β are oxysterol-activated nuclear receptors involved in the control of lipid metabolism and inflammation. Pharmacological activation of LXR is promising in the treatment of atherosclerosis since it can promote cholesterol efflux from macrophages and prevent foam cell formation. However, the development of LXR agonists has been limited by undesirable side-effects such as hepatic steatosis mediated by LXRα activation. Therefore, it has been proposed that targeting LXRα activators to extrahepatic tissues or using LXRβ-specific activators could be used as alternative strategies. It is not clear whether these molecules will retain the full atheroprotective potentia…

Apolipoprotein Emedicine.medical_specialtyBenzylaminesOxysterolHydrocarbons FluorinatedPrimary Cell CultureBiochemistryBenzoatesApolipoproteins EInternal medicinemedicineHumansRNA Small InterferingReceptorLiver X receptorCells CulturedFoam cellLiver X ReceptorsPharmacologySulfonamidesbiologyApolipoprotein A-IMacrophagesOrphan Nuclear ReceptorsLipoproteins HDL2Cell biologyEndocrinologyCholesterolABCG1Nuclear receptorABCA1Gene Knockdown Techniquesbiology.proteinlipids (amino acids peptides and proteins)Biochemical pharmacology
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Reduced VLDL clearance in ApoeNpc1 mice is associated with increased Pcsk9 and Idol expression and decreased hepatic LDL-receptor levels

2010

Niemann-Pick type C1 (NPC1) promotes the transport of LDL receptor (LDL-R)-derived cholesterol from late endosomes/lysosomes to other cellular compartments. NPC1-deficient cells showed impaired regulation of liver_X receptor (LXR) and sterol regulatory element-binding protein (SREBP) target genes. We observed that Apoe(-/-)Npc1(-/-) mice displayed a marked increase in total plasma cholesterol mainly due to increased VLDL, reflecting decreased clearance. Although nuclear SREBP-2 and Ldlr mRNA levels were increased in Apoe(-/-)Npc1(-/-) liver, LDL-R protein levels were decreased in association with marked induction of proprotein convertase subtilisin/kexin type 9 (Pcsk9) and inducible degrade…

Apolipoprotein EreceptorCholesterol VLDLLDL/metabolismMacrophages Peritoneal/cytologyBiochemistryMiceEndocrinologyhemic and lymphatic diseasesReceptorsOrphan Nuclear Receptors/geneticspolycyclic compoundsnuclear receptorCells CulturedResearch ArticlesLiver X ReceptorsMice KnockoutCulturedSterol Regulatory Element Binding Protein 2/geneticslipoproteinSerine EndopeptidasesIntracellular Signaling Peptides and ProteinsLamin Type AOrphan Nuclear ReceptorsTriglycerides/bloodCholesterolLiverProteins/geneticsKexinlipids (amino acids peptides and proteins)Proprotein ConvertasesProprotein Convertase 9Sterol Regulatory Element Binding Protein 1Niemann-Pick diseaseSterol Regulatory Element Binding Protein 2medicine.medical_specialtyCellsKnockoutUbiquitin-Protein LigasesReceptors LDL/metabolismSerine Endopeptidases/geneticsQD415-436BiologyCholesterol/blooddigestive systemApolipoproteins ELiver/physiologySterol Regulatory Element Binding Protein 1/geneticsNiemann-Pick C1 ProteinInternal medicinemedicineAnimalsPeritoneal/cytologyCholesterol VLDL/metabolismUbiquitin-Protein Ligases/geneticsLiver X receptorTriglyceridesMacrophagesPCSK9Proteinsnutritional and metabolic diseasesVLDL/metabolismLamin Type A/metabolismCell BiologySterol regulatory element-binding proteinEndocrinologyReceptors LDLLDL receptorMacrophages PeritonealSterol regulatory element-binding protein 2atherosclerosisApolipoproteins E/geneticsLipoproteinJournal of Lipid Research
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Polyamines Impair Immunity to Helicobacter pylori by Inhibiting L-Arginine Uptake Required for Nitric Oxide Production

2010

International audience; BACKGROUND & AIMS: Helicobacter pylori-induced immune responses fail to eradicate the bacterium. Nitric oxide (NO) can kill H pylori. However, translation of inducible NO synthase (iNOS) and NO generation by H pylori-stimulated macrophages is inhibited by the polyamine spermine derived from ornithine decarboxylase (ODC), and is dependent on availability of the iNOS substrate L-arginine (L-Arg). We determined if spermine inhibits iNOS-mediated immunity by reducing L-Arg uptake into macrophages. METHODS: Levels of the inducible cationic amino acid transporter (CAT) 2, ODC, and iNOS were measured in macrophages and H pylori gastritis tissues. L-Arg uptake, iNOS expressi…

ArginineSpermineNitric Oxide Synthase Type IIArginineNitric OxideOrnithine DecarboxylaseArticleOrnithine decarboxylaseNitric oxideHelicobacter Infections03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineImmune systemGastric mucosamedicinePolyaminesAnimalsHumansCationic Amino Acid Transporter 2Cells Cultured030304 developmental biology0303 health sciencesImmunity CellularHepatologybiologyHelicobacter pyloriReverse Transcriptase Polymerase Chain ReactionMacrophagesGastroenterology[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyHelicobacter pyloribiology.organism_classificationMolecular biologyMice Inbred C57BLDisease Models Animalmedicine.anatomical_structurechemistryGene Expression RegulationGastric Mucosa030220 oncology & carcinogenesisGastritisRNASperminePolyamine
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Atherogenic properties of enzymatically degraded LDL: selective induction of MCP-1 and cytotoxic effects on human macrophages.

1998

Abstract —The mechanisms underlying the selective accumulation of macrophages in early atherosclerotic lesions are poorly understood but are likely to be related to specific properties of altered low density lipoprotein (LDL) deposited in the subendothelium. Enzymatic, nonoxidative degradation of LDL converts the lipoprotein to a potentially atherogenic moiety, enzymatically altered LDL (E-LDL), which activates complement and is rapidly taken up by human macrophages via a scavenger receptor–dependent pathway. Immunohistological evidence indicates that E-LDL is present in an extracellular location in the early lesion. We report that E-LDL causes massive release of monocyte chemotactic prote…

ArteriosclerosisHydrolasesGene ExpressionNeuraminidaseBiologyCCL2Polymerase Chain Reactionchemistry.chemical_compoundExtracellularmedicineMacrophageHumansTrypsinInterleukin 8RNA MessengerCells CulturedChemokine CCL2Cell DeathMonocyteMacrophagesRNA-Directed DNA PolymeraseSterol EsteraseMolecular biologyLipoproteins LDLKineticsmedicine.anatomical_structureBiochemistrychemistryApoptosisLow-density lipoproteinlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineLipoproteinArteriosclerosis, thrombosis, and vascular biology
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Complement and atherogenesis: The unknown connection

1999

The question why low-density lipoprotein (LDL) stranded in the subendothelium of arteries should acquire the proinflammatory properties that initiate and sustain atherogenesis has puzzled researchers for decades. The most popular concept contends that oxidative processes are crucial because oxidized LDL (ox-LDL) produced in vitro has atherogenic properties and small amounts of it are found in atherosclerotic lesions. Recently, a possible role for vascular infections has also been considered because infectious agents, in particular Chlamydia pneumoniae, are sometimes present in the lesions. Here, evidence is summarized for a different concept of atherogenesis, which evolves from the fact tha…

ArteriosclerosisVascular diseaseInflammationGeneral MedicineChlamydia InfectionsChlamydophila pneumoniaeMacrophage ActivationBiologymedicine.diseaseProinflammatory cytokineLipoproteins LDLPathogenesischemistry.chemical_compoundImmune systemchemistryLow-density lipoproteinImmunologymedicineHumansMacrophagelipids (amino acids peptides and proteins)medicine.symptomComplement ActivationLipoproteinAnnals of Medicine
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Modulation of dendritic cells and macrophages : implication in cancer and atherosclerosis

2010

During my thesis, I studied the cytotoxic function of dendritic cells (DC) from cancer patients and compared it to DC from healthy donors. Our results indicate that human monocyte-derived DC can acquire strong cytotoxic activity toward tumor cells after activation with low dose of LPS. The cytotoxic potential of DC derived from cancer patients was almost the same as the one generated from healthy donors. We identified the tumor cell killing mechanism which involves peroxynitrite release. After killing of cancer cells, DC are capable of engulfing dead tumor cell fragments and overexpress the costimulatory molecules necessary for T cell proliferation. A second study consisted in an analysis o…

Athérosclérose[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyCellules dendritiquesMacrophages[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyDentritic cellslipids (amino acids peptides and proteins)Atherosclerosis[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyCancer
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