Search results for "MACROPHAGES"

showing 10 items of 533 documents

Epithelium‐specific MyD88 signaling, but not DCs or macrophages, control acute intestinal infection with Clostridium difficile

2019

Infection with Clostridium difficile is one of the major causes of health care acquired diarrhea and colitis. Signaling though MyD88 downstream of TLRs is critical for initiating the early protective host response in mouse models of C. difficile infection (CDI). In the intestine, MyD88 is expressed in various tissues and cell types, such as the intestinal epithelium and mononuclear phagocytes (MNP), including DC or macrophages. Using a genetic gain-of-function system, we demonstrate here that restricting functional MyD88 signaling to the intestinal epithelium, but also to MNPs is sufficient to protect mice during acute CDI by upregulation of the intestinal barrier function and recruitment o…

0301 basic medicineCell typeImmunologyBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationmedicineAnimalsImmunology and AllergyIntestinal MucosaColitisEnterocolitis PseudomembranousBarrier functionClostridioides difficileMacrophagesDendritic CellsClostridium difficilemedicine.diseaseIntestinal epitheliumPhenotypeEpitheliumDisease Models Animal030104 developmental biologymedicine.anatomical_structureHost-Pathogen InteractionsMyeloid Differentiation Factor 88ImmunologySignal Transduction030215 immunologyEuropean Journal of Immunology
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The activation of Wnt signaling by a STAT6-dependent macrophage phenotype promotes mucosal repair in murine IBD

2016

The complete repair of the mucosa constitutes a key goal in inflammatory bowel disease (IBD) treatment. The Wnt signaling pathway mediates mucosal repair and M2 macrophages that coordinate efficient healing have been related to Wnt ligand expression. Signal transducer and activator of transcription 6 (STAT6) mediates M2 polarization in vitro and we hypothesize that a STAT6-dependent macrophage phenotype mediates mucosal repair in acute murine colitis by activating the Wnt signaling pathway. Our results reveal an impaired mucosal expression of M2 macrophage-associated genes and delayed wound healing in STAT6(-/-) mice treated with 2,4,6-trinitrobenzenesulfonic acid (TNBS). These mice also ex…

0301 basic medicineCellular differentiationImmunologyBiology03 medical and health sciencesMice0302 clinical medicineImmunology and AllergyAnimalsHumansIntestinal MucosaCells CulturedSTAT6Mice KnockoutMice Inbred BALB CWound HealingWnt signaling pathwayLGR5LRP5Cell DifferentiationColitisInflammatory Bowel DiseasesCell biologyWnt Proteins030104 developmental biologyPhenotypeTrinitrobenzenesulfonic AcidImmunologySTAT proteinMacrophages PeritonealSignal transductionWound healingSTAT6 Transcription Factor030215 immunologySignal Transduction
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Overview of General and Discriminating Markers of Differential Microglia Phenotypes.

2020

Inflammatory processes and microglia activation accompany most of the pathophysiological diseases in the central nervous system. It is proven that glial pathology precedes and even drives the development of multiple neurodegenerative conditions. A growing number of studies point out the importance of microglia in brain development as well as in physiological functioning. These resident brain immune cells are divergent from the peripherally infiltrated macrophages, but their precise in situ discrimination is surprisingly difficult. Microglial heterogeneity in the brain is especially visible in their morphology and cell density in particular brain structures but also in the expression of cell…

0301 basic medicineCentral nervous systemInflammationReviewBiologylcsh:RC321-571M1/M2 phenotype03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineImmune systemneurotoxicitymedicineCytotoxic T celllcsh:Neurosciences. Biological psychiatry. NeuropsychiatrypolarizationMicrogliaRegeneration (biology)Neurotoxicityinfiltrating macrophagesmedicine.diseasePhenotype030104 developmental biologymedicine.anatomical_structureinflammationCellular Neuroscienceregenerationmicroglial heterogeneitymedicine.symptomNeuroscience030217 neurology & neurosurgeryFrontiers in cellular neuroscience
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NFATc1 releases BCL6-dependent repression of CCR2 agonist expression in peritoneal macrophages fromSaccharomyces cerevisiaeinfected mice

2016

The link between the extensive usage of calcineurin (CN) inhibitors cyclosporin A and tacrolimus (FK506) in transplantation medicine and the increasing rate of opportunistic infections within this segment of patients is alarming. Currently, how peritoneal infections are favored by these drugs, which impair the activity of several signaling pathways including the Ca(++) /CN/NFAT, Ca(++) /CN/cofilin, Ca(++) /CN/BAD, and NF-κB networks, is unknown. Here, we show that Saccharomyces cerevisiae infection of peritoneal resident macrophages triggers the transient nuclear translocation of NFATc1β isoforms, resulting in a coordinated, CN-dependent induction of the Ccl2, Ccl7, and Ccl12 genes, all enc…

0301 basic medicineChemokineReceptors CCR2Calcineurin InhibitorsImmunologySaccharomyces cerevisiaeOpportunistic InfectionsCCL7MonocytesMice03 medical and health sciences0302 clinical medicineCyclosporin aAnimalsProtein IsoformsImmunology and AllergyChemokine CCL7Promoter Regions GeneticCCL12Transcription factorChemokine CCL2NFATC Transcription FactorsbiologyCalcineurinNF-kappa BNFATNFATC Transcription FactorsMonocyte Chemoattractant Proteins3. Good healthCalcineurinProtein Transport030104 developmental biology030220 oncology & carcinogenesisMacrophages PeritonealProto-Oncogene Proteins c-bcl-6biology.proteinCancer researchEuropean Journal of Immunology
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Effect of colorectal cancer-derived extracellular vesicles on the immunophenotype and cytokine secretion profile of monocytes and macrophages.

2018

Abstract. Background Macrophages are one of the most important players in the tumor microenvironment. The polarization status of tumor associated macrophages into a pro-inflammatory type M1 or anti-inflammatory type M2 may influence cancer progression and patient survival. Extracellular vesicles (EVs) are membrane-bound vesicles containing different biomolecules that are involved in cell to cell signal transfer. Accumulating evidence suggests that cancer-derived EVs are taken up by macrophages and modulate their phenotype and cytokine profile. However, the interactions of cancer-derived EVs with monocytes and macrophages at various differentiation and polarization states are poorly understo…

0301 basic medicineDynaminsLipopolysaccharidesCell SurvivalCD14Macrophage polarizationLipopolysaccharide ReceptorsShort Reportlcsh:MedicineReceptors Cell Surfacecolorectal cancerBiochemistryMonocytesImmunophenotyping03 medical and health sciencesExtracellular VesiclesInterferon-gamma0302 clinical medicineCell Line TumormedicineCXCL10MacrophageHumansendocytosisSecretionLectins C-Typelcsh:QH573-671Molecular BiologyTumor microenvironmentlcsh:CytologyChemistryMonocyteMacrophageslcsh:RCell DifferentiationCell BiologyHLA-DR AntigenscytokinesCell biology030104 developmental biologymedicine.anatomical_structureMannose-Binding Lectins030220 oncology & carcinogenesisTetradecanoylphorbol AcetateCytokine secretionChemokinesColorectal NeoplasmsMannose ReceptorCell communication and signaling : CCS
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CNS Macrophages Control Neurovascular Development via CD95L.

2017

The development of neurons and vessels shares striking anatomical and molecular features, and it is presumably orchestrated by an overlapping repertoire of extracellular signals. CNS macrophages have been implicated in various developmental functions, including the morphogenesis of neurons and vessels. However, whether CNS macrophages can coordinately influence neurovascular development and the identity of the signals involved therein is unclear. Here, we demonstrate that activity of the cell surface receptor CD95 regulates neuronal and vascular morphogenesis in the post-natal brain and retina. Furthermore, we identify CNS macrophages as the main source of CD95L, and macrophage-specific del…

0301 basic medicineFas Ligand ProteinAngiogenesisMorphogenesisvesselmicrogliaBiologyGeneral Biochemistry Genetics and Molecular BiologyRetina03 medical and health sciencesangiogenesisMiceCell surface receptorExtracellularmedicineHuman Umbilical Vein Endothelial CellsNeuritesAnimalsHumansfas Receptorlcsh:QH301-705.5Cell ProliferationRetinaMicrogliaKinaseMacrophagesneurovascular developmentBrainNeurovascular bundle030104 developmental biologymedicine.anatomical_structurecortexsrc-Family Kinasesnervous systemlcsh:Biology (General)ImmunologySynapsesCD95CD95LNeuroscienceCNS macrophagesProtein BindingSignal TransductionCell reports
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Upgrading from iMac to iMicro

2017

In this issue of Immunity, Takata et al. (2017) describe a novel method to differentiate macrophages from iPSCs. These cells, which they call iMacs, are similar to yolk-sac-derived macrophages and are capable of undergoing terminal differentiation into tissue-resident-like macrophages in vitro and in vivo.

0301 basic medicineFetusMacrophagesCellular differentiationImmunologyCell DifferentiationBiologyCell biology03 medical and health sciencesFetus030104 developmental biologyInfectious Diseasesmedicine.anatomical_structureImmunityembryonic structuresImmunologymedicineHumansImmunology and AllergyYolk sacInduced pluripotent stem cellYolk SacImmunity
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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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Role of the DNA repair glycosylase OGG1 in the activation of murine splenocytes

2017

OGG1 (8-oxoguanine-DNA glycosylase) is the major DNA repair glycosylase removing the premutagenic DNA base modification 8-oxo-7,8-dihydroguanine (8-oxoG) from the genome of mammalian cells. In addition, there is accumulating evidence that OGG1 and its substrate 8-oxoG might function in the regulation of certain genes, which could account for an attenuated immune response observed in Ogg1-/- mice in several settings. Indications for at least two different mechanisms have been obtained. Thus, OGG1 could either act as an ancillary transcription factor cooperating with the lysine-specific demethylase LSD1 or as an activator of small GTPases. Here, we analysed the activation by lipopolysaccaride…

0301 basic medicineGuanineDNA RepairDNA repairp38 mitogen-activated protein kinasesBiologyBiochemistryDNA GlycosylasesMice03 medical and health sciencesAnimalsMolecular BiologyTranscription factorTumor Necrosis Factor-alphaKinaseActivator (genetics)MacrophagesDNACell BiologyBase excision repairMolecular biology030104 developmental biologyGene Expression RegulationDNA glycosylaseTumor necrosis factor alphaSpleenDNA DamageTranscription FactorsDNA Repair
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Macrophage type modulates osteogenic differentiation of adipose tissue MSCs

2017

Since the reconstruction of large bone defects remains a challenge, knowledge about the biology of bone healing is desirable to develop novel strategies for improving the treatment of bone defects. In osteoimmunology, macrophages are the central component in the early stage of physiological response after bone injury and bone remodeling in the late stage. During this process, a switch of macrophage phenotype from pro-inflammatory (M1) to anti-inflammatory (M2) is observed. An appealing option for bone regeneration would be to exploit this regulatory role for the benefit of osteogenic differentiation of osteoprogenitor cells (e.g., mesenchymal stem cells; MSCs) and to eventually utilize this…

0301 basic medicineHistologyMacrophageOsteoimmunologyAdipose tissueBone healingCell CommunicationBiologyBone morphogenetic protein 2Bone remodelingCell LinePathology and Forensic MedicineMSC03 medical and health sciencesCalcification PhysiologicAll institutes and research themes of the Radboud University Medical CenterOsteogenesisOsteogenic differentiationHumansBone regenerationCell ProliferationBone InjuryMacrophagesMesenchymal stem cellCell PolarityCell DifferentiationMesenchymal Stem CellsRegular ArticleCell BiologyAlkaline PhosphataseCoculture TechniquesCell biology030104 developmental biologyReconstructive and regenerative medicine Radboud Institute for Molecular Life Sciences [Radboudumc 10]Adipose TissueGene Expression RegulationCell culture modelImmunologyCytokinesBiomarkersCell and Tissue Research
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