Search results for "macrophage"

showing 10 items of 781 documents

CD16+ Macrophages Mediate Fibrosis in Inflammatory Bowel Disease.

2017

Background and Aims Fibrosis is a common complication of Crohn's disease [CD], and is related to dysregulated tissular repair following inflammation, in which macrophages play a central role. We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. In the present study, we analyse the role of STAT6-dependent macrophages in intestinal fibrosis. Methods Colitis was induced by weekly intra-rectal administration of TNBS [6 weeks] to STAT6-/- mice and wild-typ…

0301 basic medicineMaleCell CountInflammatory bowel diseaseMiceCrohn DiseaseFibrosisMacrophageIntestinal MucosaCells CulturedMice Knockouteducation.field_of_studyMice Inbred BALB Cintegumentary systemGastroenterologyGeneral MedicineColitisColonic NeoplasmsFemalemedicine.symptomMannose ReceptorAdultAdolescentColonPopulationInflammationReceptors Cell SurfaceCD1603 medical and health sciencesYoung AdultProto-Oncogene Proteinsparasitic diseasesmedicineAnimalsHumansLectins C-TypeColitiseducationInterleukin 4business.industryMacrophagesReceptors IgGmedicine.diseaseFibrosisWnt Proteins030104 developmental biologyMannose-Binding LectinsTrinitrobenzenesulfonic AcidImmunologyInterleukin-4businessSTAT6 Transcription FactorJournal of Crohn'scolitis
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The two faces of tumor-associated macrophages and their clinical significance in colorectal cancer

2019

© 2019 Pinto, Rios, Durães, Ribeiro, Machado, Mantovani, Barbosa, Carneiro and Oliveira. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

0301 basic medicineMaleColorectal cancerprognostic and tumor relapseMacrophages / immunologyhuman macrophage surface markers0302 clinical medicineTumor MicroenvironmentImmunology and AllergyColorectal Neoplasms / mortalityOriginal ResearchAged 80 and overTumor immunomodulationCD68tumor-associated macrophagesTumor-associated macrophagesTumor Microenvironment / immunologyMiddle AgedPrognosis3. Good healthMacrophage polarizationImmunohistochemistryFemaleHuman macrophage surface markerstumor immunomodulationColorectal NeoplasmsInfiltration (medical)lcsh:Immunologic diseases. AllergyAdultmacrophage polarizationImmunologyMacrophage polarizationcolorectal cancerBiologyPrognostic and tumor relapseColorectal Neoplasms / pathology03 medical and health sciencesYoung AdultImmune systemmedicineHumansAgedMacrophagesColorectal Neoplasms / immunologymedicine.diseaseColorectal cancer030104 developmental biologyCancer researchlcsh:RC581-607CD163CD80030215 immunology
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Interleukin-25 Axis Is Involved in the Pathogenesis of Human Primary and Experimental Murine Sjögren's Syndrome

2018

Objective To investigate the role of the interleukin-25 (IL-25)/IL-17 receptor B (IL-17RB) axis in experimental Sjogren's syndrome (SS) and in patients with primary SS and primary SS-associated lymphoma. Methods Expression of IL-25, IL-17RB, IL-17B, and tumor necrosis factor receptor-associated factor 6 (TRAF6) was analyzed on minor salivary gland (SG) samples from patients with primary SS and on parotid gland samples from patients with primary SS-associated B cell non-Hodgkin's lymphoma (NHL). IL-17RB expression and the frequencies of natural group 2 innate lymphoid cells (ILC2s), inflammatory ILC2s, and M2-polarized macrophages were assessed by flow cytometry in SG mononuclear cells and p…

0301 basic medicineMaleLymphomaMacrophageImmunologyPeripheral blood mononuclear cellSalivary GlandSalivary GlandsFlow cytometry03 medical and health sciencesMice0302 clinical medicineRheumatologyInterleukin 25AnimalsHumansMedicineImmunology and AllergyLymphocytesB cellAgedReceptors Interleukin-17medicine.diagnostic_testbusiness.industryAnimalMacrophagesInnate lymphoid cellInterleukin-17Middle Agedmedicine.diseaseImmunity InnateLymphomaSettore MED/16 - Reumatologia030104 developmental biologymedicine.anatomical_structureSjogren's SyndromeImmunologyImmunology and Allergy; Rheumatology; ImmunologyLeukocytes MononuclearRituximabTumor necrosis factor alphaFemaleLymphocytebusiness030215 immunologymedicine.drugHuman
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CAMKIIγ suppresses an efferocytosis pathway in macrophages and promotes atherosclerotic plaque necrosis

2017

Atherosclerosis is the underlying etiology of cardiovascular disease, the leading cause of death worldwide. Atherosclerosis is a heterogeneous disease in which only a small fraction of lesions lead to heart attack, stroke, or sudden cardiac death. A distinct type of plaque containing large necrotic cores with thin fibrous caps often precipitates these acute events. Here, we show that Ca2+/calmodulin-dependent protein kinase gamma (CaMKII gamma) in macrophages plays a major role in the development of necrotic, thin-capped plaques. Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation of CaMKII. We…

0301 basic medicineMalePathologymedicine.medical_specialtyPhagocytosisGene ExpressionInflammationApoptosisMice TransgenicBiologyPHAGOCYTOSISLIPID MEDIATORS03 medical and health sciencesNecrosisENDOPLASMIC-RETICULUM STRESSINFLAMMATIONCa2+/calmodulin-dependent protein kinaseC/EBP HOMOLOGOUS PROTEINmedicineMacrophageAnimalsHumansKINASE-IILiver X receptorEfferocytosisCells CulturedLiver X ReceptorsAPOE-DEFICIENT MICEc-Mer Tyrosine KinaseATF6MacrophagesAPOPTOTIC CELL ACCUMULATIONGeneral MedicineMERTKAtherosclerosisPlaque AtheroscleroticActivating Transcription Factor 6Enzyme ActivationMice Inbred C57BL030104 developmental biologyRESOLUTIONmedicine.symptomCalcium-Calmodulin-Dependent Protein Kinase Type 2LIVER-X-RECEPTORResearch ArticleSignal TransductionJournal of Clinical Investigation
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Endocannabinoid 2-arachidonoylglycerol is elevated in the coronary circulation during acute coronary syndrome

2019

Objectives The endocannabinoid system modulates coronary circulatory function and atherogenesis. The two major endocannabinoids (eCB), 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamide (AEA), are increased in venous blood from patients with coronary artery disease (CAD). However, given their short half-life and their autocrine/paracrine mechanism of action, eCB levels in venous blood samples might not reflect arterial or coronary eCB concentrations. The aim of this cross-sectional study was to identify the local concentration profile of eCB and to detect whether and how this concentration profile changes in CAD and NSTEMI versus patients without CAD. Methods and results 83 patien…

0301 basic medicineMalePhysiologyMyocardial InfarctionCoronary Artery Disease030204 cardiovascular system & hematologyCoronary AngiographyVascular MedicineBiochemistryCoronary artery disease0302 clinical medicineMedicine and Health SciencesMedicineCoronary Heart DiseaseMyocardial infarctionNon-ST Elevated Myocardial InfarctionCoronary ArteriesAortaAged 80 and overMultidisciplinaryArachidonic AcidQREukaryotaNeurochemistryVenous bloodArteriesPlantsMiddle AgedLegumesLipidsCoronary VesselsBody Fluidsmedicine.anatomical_structureBloodCirculatory systemCardiologyMedicineArterial bloodEngineering and TechnologyFemaleAnatomyNeurochemicalsResearch ArticleBiotechnologyAcute coronary syndromemedicine.medical_specialtyCathetersScienceCardiologyBioengineeringArachidonic AcidsGlyceridesDiagnosis Differential03 medical and health sciencesCoronary circulationInternal medicineCoronary CirculationHumansAcute Coronary SyndromeAgedbusiness.industryMacrophagesOrganismsPeasBiology and Life Sciencesmedicine.diseaseCoronary arteries030104 developmental biologyCross-Sectional StudiesCardiovascular AnatomyBlood VesselsMedical Devices and EquipmentEndothelium VascularbusinessEndocannabinoidsNeurosciencePLoS ONE
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Adipocyte cannabinoid receptor CB1 regulates energy homeostasis and alternatively activated macrophages.

2017

Dysregulated adipocyte physiology leads to imbalanced energy storage, obesity, and associated diseases, imposing a costly burden on current health care. Cannabinoid receptor type-1 (CB1) plays a crucial role in controlling energy metabolism through central and peripheral mechanisms. In this work, adipocyte-specific inducible deletion of the CB1 gene (Ati-CB1- KO) was sufficient to protect adult mice from diet-induced obesity and associated metabolic alterations and to reverse the phenotype in already obese mice. Compared with controls, Ati-CB1-KO mice showed decreased body weight, reduced total adiposity, improved insulin sensitivity, enhanced energy expenditure, and fat depot-specific cell…

0301 basic medicineMalemedicine.medical_specialtyCannabinoid receptorMacrophageAdipose Tissue WhiteAdipose tissueEnergy homeostasisMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineReceptor Cannabinoid CB1Internal medicineAdipocyteBrown adipose tissueHomeostasiCannabinoid receptor type 2medicineAdipocytesAnimalsHomeostasisObesityCannabisMice KnockoutAdipocyteAnimalMedicine (all)MacrophagesBody WeightGeneral MedicineMacrophage ActivationEndocannabinoid systemMice Inbred C57BL030104 developmental biologyEndocrinologymedicine.anatomical_structurechemistryOrgan SpecificityCommentaryEnergy IntakeEnergy MetabolismTranscriptome030217 neurology & neurosurgeryHomeostasisResearch ArticleThe Journal of clinical investigation
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Fate-Mapping of GM-CSF Expression Identifies a Discrete Subset of Inflammation-Driving T Helper Cells Regulated by Cytokines IL-23 and IL-1β.

2019

Summary Pathogenic lymphocytes initiate the development of chronic inflammatory diseases. The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) (encoded by Csf2) is a key communicator between pathogenic lymphocytes and tissue-invading inflammatory phagocytes. However, the molecular properties of GM-CSF-producing cells and the mode of Csf2 regulation in vivo remain unclear. To systematically study and manipulate GM-CSF+ cells and their progeny in vivo, we generated a fate-map and reporter of GM-CSF expression mouse strain (FROG). We mapped the phenotypic and functional profile of auto-aggressive T helper (Th) cells during neuroinflammation and identified the signature and pa…

0301 basic medicineMalemedicine.medical_treatmentImmunologyInterleukin-1betaInflammation610 Medicine & health10071 Functional Genomics Center ZurichBiology10263 Institute of Experimental Immunology03 medical and health sciencesInterferon-gammaMice0302 clinical medicineFate mappingImmunopathologymedicineInterleukin 23Immunology and AllergyAnimalsReceptorNeuroinflammationReceptors CXCR6InflammationMice KnockoutReceptors Interleukin-1 Type I2403 ImmunologyTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesReceptors InterleukinTh1 CellsPhenotype3. Good healthCell biology10040 Clinic for NeurologyMice Inbred C57BL030104 developmental biologyInfectious DiseasesCytokine030220 oncology & carcinogenesis2723 Immunology and AllergyInterleukin-23 Subunit p19570 Life sciences; biologyTh17 CellsFemalemedicine.symptomImmunity
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Renal tubular epithelial cell-derived BAFF expression mediates kidney damage and correlates with activity of proliferative lupus nephritis in mouse a…

2017

B-cell activating factor of the tumour necrosis factor family (BAFF) is a cytokine, mainly produced by hematopoietic cells (e.g. monocytes/macrophages, dendritic cells), indispensable for B-cell maturation. The BLISS studies have demonstrated that blocking BAFF by the human monoclonal antibody belimumab is a valuable therapeutic approach in patients with clinically and serologically active systemic lupus erythematosus (SLE). However, the defined sources of BAFF, which contributes to SLE, are still unclear. Recent findings show that BAFF expression is not restricted to myeloid cells. Since lupus nephritis is the main cause of morbidity and mortality for SLE patients, the aim of this study wa…

0301 basic medicineMalemedicine.medical_treatmentLupus nephritisAntibodies Monoclonal HumanizedKidneySeverity of Illness IndexPathogenesis03 medical and health sciencesMice0302 clinical medicinestomatognathic systemRheumatologyimmune system diseasesB-Cell Activating FactormedicineAnimalsHumansLupus Erythematosus Systemicskin and connective tissue diseasesB-cell activating factorAutocrine signallingRetrospective StudiesB-Lymphocytesbusiness.industryTumor Necrosis Factor-alphaEpithelial Cellsmedicine.diseaseBelimumabLupus Nephritisstomatognathic diseasesHaematopoiesis030104 developmental biologyCytokineReceptors Granulocyte-Macrophage Colony-Stimulating FactorImmunologyCytokinesTumor necrosis factor alphaFemaleKidney DiseasesbusinessImmunosuppressive Agents030215 immunologymedicine.drugLupus
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IL-34–Dependent Intrarenal and Systemic Mechanisms Promote Lupus Nephritis in MRL-Faslpr Mice

2019

Background In people with SLE and in the MRL- Fas lpr lupus mouse model, macrophages and autoantibodies are central to lupus nephritis. IL-34 mediates macrophage survival and proliferation, is expressed by tubular epithelial cells (TECs), and binds to the cFMS receptor on macrophages and to a newly identified second receptor, PTPRZ. Methods To investigate whether IL-34–dependent intrarenal and systemic mechanisms promote lupus nephritis, we compared lupus nephritis and systemic illness in MRL- Fas lpr mice expressing IL-34 and IL-34 knockout (KO) MRL- Fas lpr mice. We also assessed expression of IL-34 and the cFMS and PTPRZ receptors in patients with lupus nephritis. Results Intrarenal IL-3…

0301 basic medicineMice Inbred MRL lprChemokineCell SurvivalLupus nephritisRisk AssessmentMonocytesMice03 medical and health sciences0302 clinical medicineSpecies Specificityimmune system diseasesmedicineAnimalsMacrophageMolecular Targeted Therapyskin and connective tissue diseasesCells CulturedCell ProliferationMice KnockoutSystemic lupus erythematosusCell Deathbiologybusiness.industryInterleukinsMacrophagesGeneral MedicineMonocyte proliferationmedicine.diseaseLupus NephritisMice Inbred C57BLDisease Models AnimalBasic ResearchKidney Tubules030104 developmental biologyGene Expression RegulationNephrology030220 oncology & carcinogenesisImmunologyKnockout mouseDisease Progressionbiology.proteinChemokinesbusinessMacrophage proliferationNephritisJournal of the American Society of Nephrology
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miR-1207-5p Can Contribute to Dysregulation of Inflammatory Response in COVID-19 via Targeting SARS-CoV-2 RNA

2020

The present study focuses on the role of human miRNAs in SARS-CoV-2 infection. An extensive analysis of human miRNA binding sites on the viral genome led to the identification of miR-1207-5p as potential regulator of the viral Spike protein. It is known that exogenous RNA can compete for miRNA targets of endogenous mRNAs leading to their overexpression. Our results suggest that SARS-CoV-2 virus can act as an exogenous competing RNA, facilitating the over-expression of its endogenous targets. Transcriptomic analysis of human alveolar and bronchial epithelial cells confirmed that the CSF1 gene, a known target of miR-1207-5p, is over-expressed following SARS-CoV-2 infection. CSF1 enhances macr…

0301 basic medicineMicrobiology (medical)030106 microbiologyImmunologylcsh:QR1-502miRNA target predictionInflammationMiRNA bindingEndogenyBiologyMicrobiologylcsh:MicrobiologyVirusTranscriptome03 medical and health sciencesmacrophage recruitmentmicroRNAmedicinecompeting RNAsGenemicroRNA regulatory networkSARS-CoV-2fungiRNAinflammatory responseCell biology030104 developmental biologyInfectious Diseasesmedicine.symptomFrontiers in Cellular and Infection Microbiology
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