Search results for "macrophage"

showing 10 items of 781 documents

Extracellular vesicles do not mediate the anti-inflammatory actions of mouse-derived adipose tissue mesenchymal stem cells secretome

2021

Este artículo se encuentra disponible en la siguiente URL: https://www.mdpi.com/1422-0067/22/3/1375 Este artículo pertenece al número especial "The Role of Mesenchymal Stem Cells on Inflammatory and Fibrotic Diseases". Adipose tissue represents an abundant source of mesenchymal stem cells (MSC) for therapeutic purposes. Previous studies have demonstrated the anti-inflammatory potential of adipose tissue-derived MSC (ASC). Extracellular vesicles (EV) present in the conditioned medium (CM) have been shown to mediate the cytoprotective effects of human ASC secretome. Nevertheless, the role of EV in the anti-inflammatory effects of mouse-derived ASC is not known. The current study has investiga…

LipopolysaccharidesMaleChemokineLipopolysaccharideCélulas madre - Uso terapéutico.Adipose tissueInflammationmacrophageArticleCatalysisNitric oxideStem cells - Therapeutic use.lcsh:ChemistryInorganic ChemistryMicechemistry.chemical_compoundmedicineAnimalsMacrophageInflamación - Tratamiento.mesenchymal stem cells secretomePhysical and Theoretical ChemistryMacrophages.Receptorlcsh:QH301-705.5Molecular BiologyCells CulturedSpectroscopybiologyChemistryInflammation - Treatment.MacrophagesOrganic ChemistryMesenchymal stem cellmouse-derived adipose tissueMesenchymal Stem CellsGeneral MedicineAdipose tissues - Therapeutic use.Computer Science ApplicationsCell biologylcsh:Biology (General)lcsh:QD1-999inflammationMacrófagos.biology.proteinTejido adiposo - Uso terapéutico.medicine.symptomextracellular vesicles
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Budlein A from Viguiera robusta inhibits leukocyte-endothelial cell interactions, adhesion molecule expression and inflammatory mediators release

2009

Budlein A has been reported to exert some analgesic and anti-inflammatory properties. In this study, we have evaluated its effect on LPS-induced leukocyte recruitment in vivo and the mechanisms involved in its anti-inflammatory activity. In vivo, intravital videomicroscopy was used to determine the effects of budlein A on LPS-induced leukocyte-endothelial cell interactions in the murine cremasteric microcirculation. In vitro, the effects of budlein A on LPS-induced cytokine, chemokine and nitrites release, T-cell proliferative response as well as cell adhesion molecule expression (CAM) were evaluated. In vivo, intraperitoneal administration of budlein A (2.6 mM/kg) caused a significant redu…

LipopolysaccharidesMaleChemokineT-Lymphocytesmedicine.medical_treatmentPharmaceutical ScienceLeukocyte RollingCell CommunicationAsteraceaeNitric OxideDexamethasoneCell LineLactonesMiceIn vivoDrug DiscoverymedicineAnimalsHumansLeukocyte RollingInterleukin 8NitritesCell ProliferationPharmacologyMice Inbred BALB CbiologyPlant ExtractsCell adhesion moleculeMacrophagesMicrocirculationMonocyteEndothelial CellsCell biologyMice Inbred C57BLEndothelial stem cellmedicine.anatomical_structureCytokineComplementary and alternative medicinebiology.proteinMolecular MedicineChemokinesCell Adhesion MoleculesSesquiterpenesImmunosuppressive AgentsPhytomedicine
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CD11c+ Alveolar Macrophages are a Source of IL-23 During Lipopolysaccharide-Induced Acute Lung Injury

2013

Acute lung injury (ALI) is a severe pulmonary disease causing high numbers of fatalities worldwide. Innate immune responses are an integral part of the pathophysiologic events during ALI. Interleukin 23 (IL-23) is a proinflammatory mediator known to direct the inflammatory responses in various settings of infection, autoimmunity, and cancer. Interleukin 23 has been associated with proliferation and effector functions in T(H)17 cells. Surprisingly, little is known about production of IL-23 during ALI. In this study, we found expression of mRNA for IL-23p19 to be 10-fold elevated in lung homogenates of C57BL/6 mice after lipopolysaccharide (LPS)-induced ALI. Likewise, concentrations of IL-23 …

LipopolysaccharidesMaleLipopolysaccharideAcute Lung InjuryCD11cBiologyLung injuryCritical Care and Intensive Care MedicineInterleukin-23ArticleProinflammatory cytokineMicechemistry.chemical_compoundMacrophages AlveolarmedicineAnimalsInnate immune systemmedicine.diagnostic_testrespiratory systemCD11c Antigenrespiratory tract diseasesBronchoalveolar lavagechemistryImmunologyEmergency MedicineAlveolar macrophageInterleukin 17Shock
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HSP60 and CpG-DNA-oligonucleotides differentially regulate LPS-tolerance of hepatic Kupffer cells

2004

Background/aims: Hepatic Kupffer cells (KC) are major regulators of the immune response to gut-derived bacterial products; uncontrolled activation of KC by bacterial components is of pathogenic relevance in alcoholic hepatitis and septic shock. Methods: We examined the role of bacterial lipopolysaccharide (LPS), bacterial and autologous HSP60 and bacterial DNA, which are recognized by innate Toll-like receptors, during activation of murine KC. Results: In cultivated KC, autologous HSP60 induced a state of LPS-hyporesponsiveness; bacterial DNA did not mitigate the response to subsequent LPS-challenge in vitro; in contrast, pre-treatment of mice with bacterial DNA even significantly increased…

LipopolysaccharidesMaleLipopolysaccharideKupffer CellsImmunologyGene ExpressionGalactosamineReceptors Cell SurfaceCell LineMicrobiologyMicechemistry.chemical_compoundImmune systemImmunityHeat shock proteinAnimalsImmunology and AllergyInterleukin 6Cells CulturedbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaAlanine TransaminaseChaperonin 60Macrophage ActivationToll-Like Receptor 9DNA-Binding ProteinsToll-Like Receptor 4LiverOligodeoxyribonucleotideschemistryToll-Like Receptor 9Immunologybiology.proteinFemaleHSP60Tumor necrosis factor alphaLiver FailureImmunology Letters
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Nitric oxide synthase activity is inducible in rat, but not rabbit alveolar macrophages, with a concomitant reduction in arginase activity

1995

Alveolar macrophages were obtained by broncho-alveolar lavage of isolated rat and rabbit lungs and cultured (2.5 × 106 cells/dish) for 18 h in the absence or presence of bacterial lipopolysaccharides (LPS) alone or in combination with cytokines. Thereafter, accumulation of 3H-citrulline (NO synthase activity) and 3H-ornithine (arginase activity) were determined. During incubation of rat alveolar macrophages with 3H-arginine clear amounts of 3H-citrulline and 3H-ornithine (3.8 and 4.6% of the added 3H-arginine, respectively) were formed and most of these metabolites appeared in the incubation medium (ratios extra-/intracellular of 17 and 70 for 3H-citrulline and 3H-ornithine, respectively). …

LipopolysaccharidesMaleOrnithinemedicine.medical_specialtyArginineIn Vitro TechniquesArginineNitric OxideDexamethasoneNitric oxideRats Sprague-Dawleychemistry.chemical_compoundInternal medicineMacrophages AlveolarmedicineCitrullineAnimalsNitritesPharmacologyomega-N-MethylarginineArginasebiologyGeneral MedicineRatsArginaseNitric oxide synthaseEndocrinologychemistryEnzyme InductionOrnithine transportbiology.proteinCitrullineCytokinesFemaleTumor necrosis factor alphaAmino Acid OxidoreductasesRabbitsNitric Oxide SynthaseIntracellularNaunyn-Schmiedeberg's Archives of Pharmacology
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Cationic Proteins Inhibit l-Arginine Uptake in Rat Alveolar Macrophages and Tracheal Epithelial Cells

1999

Eosinophil-derived cationic proteins play an essential role in the pathogenesis of bronchial asthma. We tested whether cationic proteins interfere with the cationic amino-acid transport in alveolar macrophages (AMPhi) and tracheal epithelial cells, and whether L-arginine-dependent pathways were affected. The effect of cationic polypeptides on cellular uptake of [(3)H]-L-arginine, nitrite accumulation, and the turnover of [(3)H]-L-arginine by nitric oxide (NO) synthase and arginase (formation of [(3)H]-L-citrulline and [(3)H]-L-ornithine, respectively) were studied. Poly-L-arginine reduced [(3)H]-L-arginine uptake in rat AMPhi and tracheal epithelial cells in a concentration-dependent manner…

LipopolysaccharidesMalePulmonary and Respiratory MedicineTime FactorsClinical BiochemistryGene ExpressionArginineNitric OxideNitric oxideRats Sprague-DawleyPathogenesischemistry.chemical_compoundRibonucleasesFibrinolytic AgentsMacrophages AlveolarAnimalsNitriteLungMolecular BiologyNitritesArginaseDose-Response Relationship DrugbiologyATP synthaseHeparinLysineCationic polymerizationEpithelial CellsBlood ProteinsCell BiologyEosinophil Granule ProteinsProtamineRatsTracheaArginaseBiochemistrychemistryMajor basic proteinbiology.proteinCitrullineFemaleAmerican Journal of Respiratory Cell and Molecular Biology
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ttCH, a selective inhibitor of inducible nitric oxide synthase expression with antiarthritic properties

2003

In a previous work, we investigated the effects of a series of dimethoxy- and trimethoxychalcone derivatives, with various patterns of fluorination, on nitric oxide production in lipopolysaccharide-stimulated murine RAW 264.7 cells. The present study was designed to determine if 2,4,6-trimethoxy-2'-trifluoromethylchalcone (ttCH) could modulate the production of nitric oxide (NO) and/or prostaglandins in vitro and in vivo. On the mouse macrophage cell line RAW 264.7, ttCH inhibited dose-dependently NO and prostaglandin E(2) production, with IC(50) in the micromolar range. This compound had no direct inhibitory effect on inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 activities. …

LipopolysaccharidesMalemedicine.medical_treatmentBlotting WesternNitric Oxide Synthase Type IIPharmacologyCarrageenanNitric OxideDinoprostoneCell LineNitric oxideMicechemistry.chemical_compoundIn vivomedicineAnimalsEdemaEnzyme InhibitorsProstaglandin E2InflammationPharmacologybiologyChemistryMacrophagesAnti-Inflammatory Agents Non-SteroidalBiological activityArthritis ExperimentalHindlimbRatsCarrageenanIsoenzymesRadiographyNitric oxide synthaseMechanism of actionBiochemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesRats Inbred Lewbiology.proteinFemaleNitric Oxide Synthasemedicine.symptomProstaglandin Emedicine.drugEuropean Journal of Pharmacology
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Modulation of Forssman Glycosphingolipid Expression by Murine Macrophages: Coinduction with Class II MHC Antigen by the Lymphokines IL4 and IL6

1990

In contrast to murine spleen M phi, resident peritoneal M phi from health mice express very little Forssman glycolipid antigen (Fo). The following experiments suggest that Fo expression by peritoneal M phi may be associated with inflammation. Balb/c and CBA/J mice were given inflammatory stimuli by i.p. injection of live BCG, thioglycollate (TG), Corynebacterium parvum (CP), proteose peptone (PP), or LPS. Control animals received pyrogen-free saline. Expression of Fo and Ia antigen by peritoneal M phi was determined by immunofluorescence after 4 d. Application of TG or CP led to an up to 30-fold increase in Fo+, Ia+ double positive M phi over that in control animals. LPS caused mainly an in…

LipopolysaccharidesMalemedicine.medical_treatmentImmunologyPriming (immunology)BiologyGlycosphingolipidsMiceColony-Stimulating FactorsAntigenAntigens HeterophilemedicineAnimalsImmunology and AllergyMacrophagePeritoneal CavityInterleukin 4Forssman AntigenMice Inbred BALB CMice Inbred C3HGlobosidesInterleukin-6Macrophage Colony-Stimulating FactorMacrophagesHistocompatibility Antigens Class IILymphokineHematologyForssman antigenCytokineImmunologyFemaleTumor necrosis factor alphaInterleukin-4Immunobiology
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Differential uptake and killing potential of Campylobacter jejuni by human peripheral monocytes/macrophages

1997

The ability of Campylobacter jejuni to survive in monocytes after phagocytic uptake was tested in a new in vitro model using adherent macrophages derived from human peripheral monocytes. The cells were stimulated with cytokines before use to ensure full phagocytic and killing activity. The kinetics of uptake and killing of bacteria was followed for 72 h with 16 strains, including stool and blood isolates and laboratory adapted strains. Significant bacterial strain differences were not observed, but the viability of phagocytosed bacteria was dependent on the individual donating the macrophages. The majority of blood donors carried macrophages that killed phagocytosed Campylobacter within 24 …

LipopolysaccharidesMicrobiology (medical)Blood Bactericidal ActivityCellular immunityPhagocytosisImmunologyColony Count MicrobialBacteremiaIn Vitro TechniquesBiologymedicine.disease_causeCampylobacter jejuniMonocytesMicrobiologyCampylobacter jejuniPhagocytosisCampylobacter InfectionsmedicineHumansImmunology and AllergyMacrophagePhosphotransferases (Phosphate Group Acceptor)Superoxide DismutaseMacrophagesMonocyteCampylobacterGeneral MedicineCatalasebiology.organism_classificationEnteritisIn vitroKineticsmedicine.anatomical_structureMutationBacteriaMedical Microbiology and Immunology
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New insight into the inhibition of the inflammatory response to experimental delayed-type hypersensitivity reactions in mice by scropolioside A.

2006

Scropolioside A, an iridoid isolated from Scrophularia auriculata ssp. pseudoauriculata, showed anti-inflammatory properties against different experimental models of delayed-type hypersensitivity. This iridoid reduced the oedema induced by oxazolone by 79% (72 h) at 0.5 mg/ear while reducing that induced by sheep red blood cells by 47% (18 h), 45% (24 h) and 36% (48 h) at 10 mg/kg. In vivo it reduced both oedema formation and cell infiltration whereas in vitro it reduced the proliferation of activated T-lymphocytes (IC50 of 67.74 microM). Treatment with scropolioside A (100 microM) 18 and 24 h after phytohemagglutinin stimulation increased the number of cells arrested in the subG(0) phase w…

LipopolysaccharidesNecrosisErythrocytesLeukotriene B4NeutrophilsT-LymphocytesAnti-Inflammatory AgentsStimulationInflammationApoptosisLymphocyte proliferationPharmacologyBiologyLeukotriene B4DinoprostoneNitric oxideCell LineOxazolonechemistry.chemical_compoundMiceGlucosidesmedicineAnimalsEdemaHumansHypersensitivity DelayedPyransPharmacologySheepPancreatic ElastaseCaspase 3MacrophagesOxazoloneEarAllergenschemistryDelayed hypersensitivityImmunologyCytokinesFemalemedicine.symptomEuropean journal of pharmacology
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