Search results for "cx3cl1"

showing 10 items of 16 documents

Cocaine-induced changes in CX3CL1 and inflammatory signaling pathways in the hippocampus: Association with IL1β

2020

Cocaine induces neuroinflammatory response and interleukin-1 beta (IL1β) is suggested a final effector for many cocaine-induced inflammatory signals. Recently, the chemokine fractalkine (CX3CL1) has been reported to regulate hippocampus-dependent neuroinflammation and synaptic plasticity via CX3C-receptor 1 (CX3CR1), but little is known about the impact of cocaine. This study is mainly focused on the characterization of CX3CL1, IL1β and relevant inflammatory signal transduction pathways in the hippocampus in acute and repeated cocaine-treated male mice. Complementarily, the rewarding properties of cocaine were also assessed in Cx3cr1-knockout (KO) mice using a conditioned place preference (…

0301 basic medicinePharmacologyChemokinemedicine.medical_specialtybiologyChemistryHippocampusCREBConditioned place preference03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biology0302 clinical medicineEndocrinologyInternal medicineCX3CR1Synaptic plasticitybiology.proteinmedicineCX3CL1030217 neurology & neurosurgeryNeuroinflammationNeuropharmacology
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Minimal hepatic encephalopathy is associated with expansion and activation of CD4+CD28−, Th22 and Tfh and B lymphocytes

2017

AbstractPeripheral inflammation acts synergistically with hyperammonemia in inducing neurological alterations in cirrhotic patients with minimal hepatic encephalopathy (MHE). We hypothesized that appearance of MHE would be associated to some specific qualitative change in peripheral inflammation. The aim of this work was to characterize the changes in peripheral inflammation associated to appearance of MHE. We analyzed it by immunophenotyping and cytokine profile analysis, in cirrhotic patients without or with MHE and controls. The main alterations associated specifically with MHE are: 1) increased activation of all subtypes of CD4+ T-lymphocytes, with the increased expression of CD69; 2) i…

0301 basic medicinemedicine.medical_specialtyScienceInflammationArticleMonocytesImmunophenotyping03 medical and health sciencesImmune systemImmunophenotypingCD28 AntigensInternal medicinemedicineHumansCX3CL1Hepatic encephalopathyB-LymphocytesMultidisciplinarybusiness.industryCD69QRCD28HyperammonemiaT-Lymphocytes Helper-Inducermedicine.disease030104 developmental biologyEndocrinologyHepatic EncephalopathyImmunoglobulin GCD4 AntigensImmunologyMedicineCytokinesmedicine.symptombusinesshuman activitiesScientific Reports
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Proinflammatory CX3CR1+CD59+Tumor Necrosis Factor–Like Molecule 1A+Interleukin‐23+ Monocytes Are Expanded in Patients With Ankylosing Spondylitis and…

2018

Objective: Gut-derived innate lymphoid cell 3 (ILC3) has been shown to participate in the pathogenesis of ankylosing spondylitis (AS). CX3CR1+ mononuclear phagocytes (MNPs) have been demonstrated to modulate ILC3 function in the gut. This study was undertaken to investigate the role of proinflammatory CX3CR1+CD59+ MNPs in modulating ILC3 function in AS patients. Methods: MNP subsets in the blood of AS patients and controls were analyzed by flow cytometry. The presence of CX3CR1+CD59+ cells in tissue was confirmed by confocal microscopy. Expression of the proinflammatory chemokines CX3CL1 and CCL2 and decoy receptor 6 (DcR-6) was analyzed. Peripheral CX3CR1+CD59+ cells were cocultured with I…

AdultMale0301 basic medicineChemokineImmunologyPopulationCX3C Chemokine Receptor 1CD11cCD59 Antigenschemical and pharmacologic phenomenaCCL2Interleukin-23MonocytesProinflammatory cytokineFlow cytometry03 medical and health sciences0302 clinical medicineRheumatologymedicineHumansImmunology and AllergySpondylitis AnkylosingLymphocytesCX3CL1educationMononuclear Phagocyte System030203 arthritis & rheumatologyeducation.field_of_studybiologymedicine.diagnostic_testChemistryInnate lymphoid cellMiddle AgedImmunity Innate030104 developmental biologyReceptors Tumor Necrosis Factor Type ICase-Control Studiesbiology.proteinCancer researchFemaleArthritis & Rheumatology
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CX3CR1/CX3CL1 Axis Mediates Platelet–Leukocyte Adhesion to Arterial Endothelium in Younger Patients with a History of Idiopathic Deep Vein Thrombosis

2018

AbstractMechanisms linking deep vein thrombosis (DVT) and subclinical atherosclerosis and risk of cardiovascular events are poorly understood. The aim of this study was to investigate the potential impact of CX3CR1/CX3CL1 axis in DVT-associated endothelial dysfunction. The study included 22 patients (age: 37.5 ± 8.2 years) with a history of idiopathic DVT and without known cardiovascular risk factors and 23 aged-matched control subjects (age: 34 ± 7.8 years). Flow cytometry was used to evaluate peripheral markers of platelet activation, leukocyte immunophenotypes and CX3CR1/CX3CL1 expression in both groups. A flow chamber assay was employed to measure leukocyte arrest under dynamic conditio…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyAdolescentEndotheliumCX3C Chemokine Receptor 1InflammationComorbidity030204 cardiovascular system & hematologyMonocytesImmunophenotypingYoung Adult03 medical and health sciencesPlatelet Adhesiveness0302 clinical medicineRisk FactorsPlatelet adhesivenessHuman Umbilical Vein Endothelial CellsLeukocytesmedicineHumansPlateletLymphocytescardiovascular diseasesPlatelet activationEndothelial dysfunctionSistema cardiovascularInflammationVenous ThrombosisChemokine CX3CL1Tumor Necrosis Factor-alphabusiness.industryEndothelial CellsHematologyMiddle AgedPlatelet Activationmedicine.diseaseThrombosis030104 developmental biologymedicine.anatomical_structureMicroscopy FluorescenceCase-Control StudiesFemaleEndothelium Vascularmedicine.symptombusinessPlatelet factor 4Thrombosis and Haemostasis
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A novel role of the CX3CR1/CX3CL1 system in the cross-talk between chronic lymphocytic leukemia cells and tumor microenvironment

2011

Several chemokines/chemokine receptors such as CCR7, CXCR4 and CXCR5 attract chronic lymphocytic leukemia (CLL) cells to specific microenvironments. Here we have investigated whether the CX(3)CR1/CX(3)CL1 axis is involved in the interaction of CLL with their microenvironment. CLL cells from 52 patients expressed surface CX(3)CR1 and CX(3)CL1 and released constitutively soluble CX(3)CL1. One third of these were attracted in vitro by soluble CX(3)CL1. CX(3)CL1-induced phosphorylation of PI3K, Erk1/2, p38, Akt and Src was involved in induction of CLL chemotaxis. Leukemic B cells upregulated CXCR4 upon incubation with CX(3)CL1 and this was paralleled by increased chemotaxis to CXCL12. Akt phosp…

AdultMalechemokines; chronic lymphocytic leukemia (CLL); nurselike cells (NLCs); tumor microenvironmentCancer ResearchChemokineStromal cellChronic lymphocytic leukemiaCX3C Chemokine Receptor 1Antigens Differentiation MyelomonocyticchemokinesC-C chemokine receptor type 7Cell Communicationnurselike cells (NLCs)Chemokine receptorAntigens CDimmune system diseaseshemic and lymphatic diseaseschronic lymphocytic leukemia (CLL)medicineHumanstumor microenvironmentPhosphorylationAgedAged 80 and overTumor microenvironmentbiologyChemokine CX3CL1ChemistryChemotaxisHematologyMiddle Agedmedicine.diseaseLeukemia Lymphocytic Chronic B-CellCX(3)CR1/CX(3)CL1 systemCX(3)CR1/CX(3)CL1 system; chronic lymphocytic leukemia.LeukemiaHaematopoiesisOncologychronic lymphocytic leukemia.Cancer researchbiology.proteinFemaleReceptors ChemokineLymph NodesProto-Oncogene Proteins c-aktSignal TransductionLeukemia
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2021

To what extent the intake of fruit and vegetables (FV) influences inflammatory status remains elusive, particularly in older populations. The aim of the present study was to determine the effect of increased FV intake for 16 weeks on circulating biomarkers of inflammation in a population of older men and women. Sixty-six participants (65–70 years) randomly assigned to either FV or control (CON) groups were instructed to increase FV intake to five servings per day through nutritional counseling (FV) or to maintain habitual diet (CON). Dietary intake and physical activity level (PA) were determined using food frequency questionnaire and accelerometers, respectively, at the start and end of th…

Chemokineeducation.field_of_studyNutrition and DieteticsWaistbiologybusiness.industryPopulationPhysiologyInflammationPhysical activity levellaw.inventionRandomized controlled triallawbiology.proteinMedicinemedicine.symptomInterleukin 6educationbusinessCX3CL1Food ScienceNutrients
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Oxytocin reverses ethanol consumption and neuroinflammation induced by social defeat in male mice

2020

Abstract Oxytocin (OXT) modulates social interactions, attenuates stressful responses and can decrease drug-seeking and taking behaviors. In previous studies, we observed that social defeat (SD) induced a long-lasting increase in ethanol intake and neuroinflammation in male mice. We also know that OXT blocks the increase in cocaine reward induced by SD. Therefore, in the present study we aimed to evaluate the effect of 1 mg/kg of OXT administered 30 min before each episode of SD on ethanol consumption and the neuroinflammatory response in adult male mice. Three weeks after the last SD, mice underwent oral ethanol self-administration (SA) procedure, and striatal levels of the two chemokines …

MaleChemokinemedicine.medical_specialtyAlcohol DrinkingSelf AdministrationOxytocinSocial DefeatSocial defeatMice03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compound0302 clinical medicineEndocrinologyNeuritisRewardInternal medicineAnimalsMedicineCX3CL1NeuroinflammationSocial stressMotivationEthanolEthanolbiologyChemokine CX3CL1Endocrine and Autonomic Systemsbusiness.industryChemokine CXCL12Corpus Striatum030227 psychiatryEndocrinologyOxytocinchemistrybiology.proteinbusinessSelf-administrationStress Psychologicalhormones hormone substitutes and hormone antagonists030217 neurology & neurosurgerymedicine.drugHormones and Behavior
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Social defeat-induced increase in the conditioned rewarding effects of cocaine: Role of CX3CL1

2019

Abstract Social stress is associated with higher vulnerability to drug use, as it enhances the reinforcing effects of psychostimulants in rodents. Furthermore, continued or severe stress induces a proinflammatory state of microglial activation and augmented cytokine production. The aim of the present work was to evaluate the role of fractalkine [C-X3-C motif ligand 1 (CX3CL1)], an inflammatory chemokine, in the increased conditioned rewarding effects of cocaine in animals exposed to social defeat stress. In addition, we measured the signaling cascade pathway of CX3CL1 in the hippocampus (HPC) (including p-ERK/ERK, p-p38/p38 MAPK, p-p65/p65 NFκB and p-CREB/CREB ratios). The glutamate recepto…

MaleMAPK/ERK pathwaymedicine.medical_specialtyCREBSocial DefeatSocial defeatMice03 medical and health sciences0302 clinical medicineCocaineDopamine Uptake InhibitorsRewardInternal medicineConditioning PsychologicalCX3CR1AnimalsMedicineCX3CL1Biological PsychiatryMice KnockoutPharmacologySocial stressbiologyChemokine CX3CL1business.industryGlutamate receptorConditioned place preference030227 psychiatryMice Inbred C57BLEndocrinologybiology.proteinbusinessProgress in Neuro-Psychopharmacology and Biological Psychiatry
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Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
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Ethanol intake in male mice exposed to social defeat: Environmental enrichment potentiates resilience

2021

Large preclinical evidence shows that exposure to social defeat (SD) increases vulnerability to drug abuse, increasing the consumption of ethanol. However, not all subjects are equally affected by the changes induced by stress. Previous reports have evidenced that the resilient phenotype to depressive-like behaviors after SD is associated with the resistant phenotype to cocaine-increased rewarding effects and the smaller neuroinflammatory response. The aim of the present study was to further clarify whether the resilient profile to depressive-like behavior also predicts a protection against the increase in ethanol intake induced by SD. The neuroinflammatory profile was studied after the end…

Neurophysiology and neuropsychologymedicine.medical_specialtyChemokinePhysiologyNeurosciences. Biological psychiatry. NeuropsychiatryStriatumBiochemistrySocial defeatCellular and Molecular NeuroscienceEndocrinologyNeuroinflammationSocial defeatInternal medicinemedicineOriginal Research ArticlePrefrontal cortexCX3CL1RC346-429Molecular BiologyNeuroinflammationSocial stressEnvironmental enrichmentbiologyEthanolResilienceEndocrine and Autonomic Systemsbusiness.industryQP351-495Environmental enrichmentEndocrinologySusceptibilitybiology.proteinNeurology. Diseases of the nervous systembusinessRC321-571Neurobiology of Stress
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