Search results for "CHEMOKINE"

showing 10 items of 372 documents

IL-6 receptor independent stimulation of human gp130 by viral IL-6.

2000

Abstract The genome of human herpes virus 8, which is associated with Kaposi’s sarcoma, encodes proteins with similarities to cytokines and chemokines including a homologue of IL-6. Although the function of these viral proteins is unclear, they might have the potential to modulate the immune system. For viral IL-6 (vIL-6), it has been demonstrated that it stimulates IL-6-dependent cells, indicating that the IL-6R system is used. IL-6 binds to IL-6R, and the IL-6/IL-6R complex associates with gp130 which dimerizes and initiates intracellular signaling. Cells that only express gp130 but no IL-6R cannot be stimulated by IL-6 unless a soluble form of the IL-6R is present. This type of signaling…

MaleSTAT3 Transcription FactorChemokinemedicine.medical_treatmentImmunologyGenetic VectorsBiologylaw.inventionViral ProteinsImmune systemlawAntigens CDmedicineCytokine Receptor gp130Tumor Cells CulturedImmunology and AllergyAnimalsChemical PrecipitationHumansCloning MolecularPhosphorylationInterleukin 6Sarcoma KaposiAgedMembrane GlycoproteinsInterleukin-6Glycoprotein 130Receptors Interleukin-6Growth InhibitorsRecombinant ProteinsCell biologyDNA-Binding ProteinsCytokineInterleukin-6 receptorCOS CellsRecombinant DNAbiology.proteinTrans-ActivatorsIntracellularProtein BindingSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
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TLR4 response mediates ethanol-induced neurodevelopment alterations in a model of fetal alcohol spectrum disorders

2017

Background Inflammation during brain development participates in the pathogenesis of early brain injury and cognitive dysfunctions. Prenatal ethanol exposure affects the developing brain and causes neural impairment, cognitive and behavioral effects, collectively known as fetal alcohol spectrum disorders (FASD). Our previous studies demonstrate that ethanol activates the innate immune response and TLR4 receptor and causes neuroinflammation, brain damage, and cognitive defects in the developmental brain stage of adolescents. We hypothesize that by activating the TLR4 response, maternal alcohol consumption during pregnancy triggers the release of cytokines and chemokines in both the maternal …

MaleSerum0301 basic medicineChemokineDevelopmental Disabilitiesmedicine.medical_treatmentlcsh:RC346-429MiceMyelin0302 clinical medicineNeuroinflammationPregnancyTLR4Maternal BehaviorFetal alcohol spectrum disordersMice KnockoutMicrogliabiologyGeneral NeuroscienceAge FactorsBrainCerebral cortexBehavior impairmentsmedicine.anatomical_structureCytokineNeurologyPrenatal Exposure Delayed EffectsCytokinesFemalemedicine.symptomMyelin ProteinsAmniotic fluidmedicine.medical_specialtyOffspringImmunologyNerve Tissue ProteinsBrain damage03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicineAvoidance LearningmedicineAnimalsMaze Learninglcsh:Neurology. Diseases of the nervous systemNeuroinflammationEthanolbusiness.industryResearchBody WeightCentral Nervous System DepressantsMice Inbred C57BLToll-Like Receptor 4Disease Models AnimalMicroscopy Electron030104 developmental biologyEndocrinologyAnimals NewbornPrenatal ethanol exposureImmunologybiology.proteinTLR4business030217 neurology & neurosurgeryJournal of Neuroinflammation
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Functional characterization of the dural sinuses as a neuroimmune interface

2021

Summary Despite the established dogma of central nervous system (CNS) immune privilege, neuroimmune interactions play an active role in diverse neurological disorders. However, the precise mechanisms underlying CNS immune surveillance remain elusive; particularly, the anatomical sites where peripheral adaptive immunity can sample CNS-derived antigens and the cellular and molecular mediators orchestrating this surveillance. Here, we demonstrate that CNS-derived antigens in the cerebrospinal fluid (CSF) accumulate around the dural sinuses, are captured by local antigen-presenting cells, and are presented to patrolling T cells. This surveillance is enabled by endothelial and mural cells formin…

MaleT-LymphocytesDura materCentral nervous systemAntigen-Presenting CellsCranial SinusesBiologyGeneral Biochemistry Genetics and Molecular BiologyMural cell03 medical and health sciences0302 clinical medicineImmune privilegemedicineAnimalsHomeostasisHumansAntigensCellular Senescence030304 developmental biologyAntigen Presentation0303 health sciencesMultiple sclerosisImmunityMeningesmedicine.diseaseAcquired immune systemResearch HighlightChemokine CXCL12Mice Inbred C57BLPhenotypeNeuroimmunologymedicine.anatomical_structureFemaleDura MaterStromal CellsNeuroscience030217 neurology & neurosurgeryCell
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Thyroid hormone induction of the adrenoleukodystrophy-related gene (ABCD2).

2003

X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VLCFA) beta-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3'-tri-iodothyronine (T3) receptor (TRbeta) as a heterodimer and mediating T3 responsiveness of ABCD2 in its promoter conte…

MaleThyroid HormonesReceptors Retinoic AcidGene ExpressionATP-binding cassette transporterRetinoid X receptorRats Sprague-DawleyMiceABCD3Gene expressionABCD2medicineAnimalsHumansReceptorAdrenoleukodystrophyPromoter Regions GeneticGeneCells CulturedRepetitive Sequences Nucleic AcidPharmacologyChemokine CCL22Mice KnockoutReceptors Thyroid Hormonebiologymedicine.diseaseCell biologyRatsUp-RegulationOligodendrogliaRetinoid X ReceptorsLiverAstrocytesChemokines CCbiology.proteinCancer researchMolecular MedicineTriiodothyronineAdrenoleukodystrophyChemokine CCL17Transcription FactorsMolecular pharmacology
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Incidence of Abcd1 level on the induction of cell death and organelle dysfunctions triggered by very long chain fatty acids and TNF-alpha on oligoden…

2012

X-linked adrenoleukodystrophy (X-ALD) is characterized by ABCD1 deficiency. This disease is associated with elevated concentrations of very long chain fatty acids (C24:0 and C26:0) in the plasma and tissues of patients. Under its severe form, brain demyelination and inflammation are observed. Therefore, we determined the effects of C24:0 and C26:0 on glial cells:oligodendrocytes, which synthesize myelin, and astrocytes, which participate in immune response. So, 158N murine oligodendrocytes, rat C6 glioma cells, rat primary cultures of neuronal-glial cells, and of oligodendrocytes were treated for various periods of time in the absence or presence of C24:0 and C26:0 used at plasmatic concent…

MaleTime FactorsVacuoleMitochondrionToxicologyATP Binding Cassette Transporter Subfamily D Member 1chemistry.chemical_compoundMice0302 clinical medicineRNA Small InterferingAdrenoleukodystrophyCells CulturedComputingMilieux_MISCELLANEOUSMembrane Potential MitochondrialNeurons0303 health sciencesGeneral NeuroscienceFatty AcidsBrainPeroxisomeCatalaseFlow Cytometry3. Good healthCell biologyMitochondriaOligodendrogliamedicine.anatomical_structureFemaleProgrammed cell deathChromatography GasBiologyGas Chromatography-Mass SpectrometryStatistics Nonparametric03 medical and health sciencesMicroscopy Electron TransmissionLysosomeOrganellemedicineAnimalsHumansPropidium iodideRNA MessengerRats Wistar030304 developmental biologyCell SizeChemokine CCL22OrganellesDose-Response Relationship DrugCell growthTumor Necrosis Factor-alphaRatschemistryAnimals NewbornAstrocytesATP-Binding Cassette Transporters[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgery
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A critical role for TNFα in the selective attachment of mononuclear leukocytes to angiotensin-II-stimulated arterioles

2007

Abstract Angiotensin II (Ang-II) exerts inflammatory activity and is involved in different cardiovascular disorders. This study has evaluated the involvement of tumor necrosis factor alpha (TNFα) in the leukocyte accumulation elicited by Ang-II. Ang-II (1 nM intraperitoneally in rats) induced TNFα release at 1 hour followed by neutrophil and mononuclear cell recruitment. The administration of an antirat TNFα antiserum had no effect on Ang-IIinduced neutrophil accumulation but inhibited the infiltration of mononuclear cells and reduced CC chemokine content in the peritoneal exudate. Pretreatment with either an anti-TNFα or an anti-IL-4 antiserum decreased Ang-II-induced arteriolar mononuclea…

MaleUmbilical Veinsmedicine.medical_specialtyEndotheliummedicine.medical_treatmentImmunologyBiologyBiochemistryPeripheral blood mononuclear cellMicrocirculationRats Sprague-DawleyInternal medicineCell AdhesionmedicineAnimalsHumansVasoconstrictor AgentsRNA MessengerVenuleReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaAngiotensin IICell BiologyHematologyAngiotensin IIRatsArteriolesMononuclear cell infiltrationmedicine.anatomical_structureCytokineEndocrinologyLeukocytes MononuclearTumor necrosis factor alphaEndothelium VascularInterleukin-4ChemokinesInjections IntraperitonealBlood
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Vitamin D Receptor Activation Reduces Angiotensin-II–Induced Dissecting Abdominal Aortic Aneurysm in Apolipoprotein E–Knockout Mice

2015

Objective— Abdominal aortic aneurysm (AAA) is a vascular disorder characterized by chronic inflammation of the aortic wall. Low concentrations of vitamin D 3 are associated with AAA development; however, the potential direct effect of vitamin D 3 on AAA remains unknown. This study evaluates the effect of oral treatment with the vitamin D 3 receptor (VDR) ligand, calcitriol, on dissecting AAA induced by angiotensin-II (Ang-II) infusion in apoE −/− mice. Approach and Results— Oral treatment with calcitriol reduced Ang-II–induced dissecting AAA formation in apoE −/− mice, which was unrelated to systolic blood pressure or plasma cholesterol concentrations. Immunohistochemistry and reverse-tran…

MaleVascular Endothelial Growth Factor A0301 basic medicineDissecting Abdominal Aortic Aneurysm030204 cardiovascular system & hematologyLigandsCalcitriol receptorchemistry.chemical_compound0302 clinical medicineAorta AbdominalCells CulturedMice KnockoutAngiotensin IIVascular endothelial growth factorChemotaxis LeukocyteVascular endothelial growth factor APhenotypeMatrix Metalloproteinase 9Vitamin D3 ReceptorMatrix Metalloproteinase 2RNA Interferencelipids (amino acids peptides and proteins)ChemokinesMitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineSignal Transductionmedicine.drugmedicine.medical_specialtyCalcitriolBiologyTransfectionProinflammatory cytokine03 medical and health sciencesApolipoproteins ECalcitriolInternal medicineHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansGenetic Predisposition to DiseaseRetinoid X Receptor alphaMacrophagesAngiotensin IIMice Inbred C57BLAortic DissectionDisease Models Animal030104 developmental biologyEndocrinologychemistryReceptors CalcitriolAortic Aneurysm AbdominalArteriosclerosis, Thrombosis, and Vascular Biology
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CXCR2 blockade impairs angiotensin II-induced CC chemokine synthesis and mononuclear leukocyte infiltration.

2007

Objective—Angiotensin II (Ang-II) and mononuclear leukocytes are involved in atherosclerosis. This study reports the inhibition of Ang-II–induced mononuclear cell recruitment by CXCR2 antagonism and the mechanisms involved.Methods and Results—Ang-II (1 nmol/L, i.p. in rats) induced CXC and CC chemokines, followed by neutrophil and mononuclear cell recruitment. Administration of the CXCR2 antagonist, SB-517785-M, inhibited the infiltration of both neutrophils (98%) and mononuclear cells (60%). SB-517785-M had no effect on the increase in CXC chemokine levels but reduced MCP-1, RANTES, and MIP-1α release by 66%, 63%, and 80%, respectively. Intravital microscopy showed that pretreatment with S…

Malemedicine.medical_specialtyChemokineCXCR3Peripheral blood mononuclear cellLosartanReceptors Interleukin-8BRats Sprague-DawleyChemokine receptorInternal medicinemedicineCell AdhesionCCL17AnimalsHumansCXC chemokine receptorsSplanchnic CirculationChemokine CCL7Chemokine CCL4Chemokine CCL5Cells CulturedChemokine CCL2Chemokine CCL3InflammationbiologyAngiotensin IIMicrocirculationEndothelial CellsMacrophage Inflammatory ProteinsAtherosclerosisAngiotensin IIMonocyte Chemoattractant ProteinsRatsMononuclear cell infiltrationChemotaxis LeukocyteEndocrinologyNeutrophil Infiltrationbiology.proteinLeukocytes MononuclearCardiology and Cardiovascular MedicineAngiotensin II Type 1 Receptor BlockersArteriosclerosis, thrombosis, and vascular biology
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Cytokine expression in tears of patients with glaucoma or dry eye disease: A prospective, observational cohort study.

2018

Background: The aim of this study was to assess the expression of cytokines/chemokines in tears from patients with non-advanced primary open-angle glaucoma and patients with non-severe dry eye disease versus healthy controls. Methods: This prospective, observational cohort study enrolled patients with confirmed or suspected non-advanced primary open-angle glaucoma who received any prostaglandin analogue monotherapy for longer than 6 months, patients with non-severe dry eye disease, and healthy controls. Expression of interleukin-1β, interleukin-2, interleukin-4, interleukin-5, interleukin-6, interleukin-8, interleukin-10, and interleukin-12; tumor necrosis factor α; vascular endothelial gro…

Malemedicine.medical_specialtyChemokineGlaucomaInflammationDiseaseCohort Studies03 medical and health sciences0302 clinical medicineOphthalmologymedicineHumansProspective StudiesEye ProteinsAntihypertensive AgentsIntraocular PressureAgedbiologybusiness.industryPreservatives PharmaceuticalCytokine expressionGeneral MedicineMiddle Agedmedicine.diseaseOphthalmologyTears030221 ophthalmology & optometrybiology.proteinTearsCytokinesDry Eye SyndromesFemalemedicine.symptomOphthalmic Solutionsbusiness030217 neurology & neurosurgeryGlaucoma Open-AngleCohort studyEuropean journal of ophthalmology
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Atorvastatin in stable angina patients lowers CCL2 and ICAM1 expression: Pleiotropic evidence from plasma mRNA analyses

2013

Objective: Statin pleiotropy is still an evolving concept, and the lack of clarity on this subject is due at least in part to the lack of a definitive biomarker for statin pleiotropy. Using plasma mRNA analysis as a novel research tool for the non-invasive in vivo assessment of gene expression in vascular beds, we hypothesised that atorvastatin lowers the plasmamRNA level from statin pleiotropy-target genes, and the reduction is independent of the reduction of low-density lipoprotein cholesterol (LDL-C). Design and methods: Forty-four patients with stable angina received atorvastatin therapy (20 mg/day, 10 weeks). Plasma chemokine (C-C motif) ligand 2 (CCL2) and intercellular adhesion molec…

Malemedicine.medical_specialtyChemokineStatinmedicine.drug_classAtorvastatinClinical BiochemistryGene ExpressionDrug Administration ScheduleIn vivoInternal medicineGene expressionAtorvastatinmedicineHumansPyrrolesAngina StableRNA MessengerSerum amyloid AChemokine CCL2AgedbiologyAnticholesteremic AgentsAtorvastatin CCL2 ICAM1 Interventional trial mRNA in plasma Pleiotropic effectsC-reactive proteinCholesterol LDLGeneral MedicineMiddle AgedIntercellular Adhesion Molecule-1EndocrinologyHeptanoic AcidsHMG-CoA reductasebiology.proteinFemalelipids (amino acids peptides and proteins)medicine.drugClinical Biochemistry
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