Search results for "CYTOKINE"

showing 10 items of 1787 documents

Nuclear Translocation of RELB Is Increased in Diseased Human Liver and Promotes Ductular Reaction and Biliary Fibrosis in Mice.

2019

Background & Aims Cholangiocyte proliferation and ductular reaction contribute to the onset and progression of liver diseases. Little is known about the role of the transcription factor nuclear factor-κB (NF-κB) in this process. We investigated the activities of the RELB proto-oncogene NF-κB subunit in human cholangiocytes and in mouse models of liver disease characterized by a ductular reaction. Methods We obtained liver tissue samples from patients with primary sclerosing cholangitis, primary biliary cholangitis, hepatitis B or C virus infection, autoimmune hepatitis, alcoholic liver disease, or without these diseases (controls) from a tissue bank in Germany. Tissues were analyzed by immu…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseaseCholangiocyte proliferationAutoimmune hepatitisProto-Oncogene MasLiver diseaseMice0302 clinical medicineCarbon TetrachlorideCells CulturedRELBLiver DiseasesGastroenterologyMiddle Aged3. Good healthDeubiquitinating Enzyme CYLDCysteine EndopeptidasesProtein TransportLiverGene Knockdown TechniquesCytokines030211 gastroenterology & hepatologyFemaleCell activationAdultLymphotoxin-betaAdolescentCholangitis SclerosingPrimary sclerosing cholangitis03 medical and health sciencesYoung AdultLymphotoxin beta ReceptormedicineAnimalsHumansRNA MessengerParenchymal TissueAgedCell ProliferationCell NucleusHepatologybusiness.industryTranscription Factor RelBEpithelial CellsDicarbethoxydihydrocollidinemedicine.diseaseFibrosis030104 developmental biologyCancer researchLiver functionBile DuctsbusinessGastroenterology
researchProduct

Loss of cellular FLICE-inhibitory protein promotes acute cholestatic liver injury and inflammation from bile duct ligation.

2017

Cholestatic liver injury results from impaired bile flow or metabolism and promotes hepatic inflammation and fibrogenesis. Toxic bile acids that accumulate in cholestasis induce apoptosis and contribute to early cholestatic liver injury, which is amplified by accompanying inflammation. The aim of the current study was to evaluate the role of the antiapoptotic caspase 8-homolog cellular FLICE-inhibitory (cFLIP) protein during acute cholestatic liver injury. Transgenic mice exhibiting hepatocyte-specific deletion of cFLIP (cFLIP−/−) were used for in vivo and in vitro analysis of cholestatic liver injury using bile duct ligation (BDL) and the addition of bile acids ex vivo. Loss of cFLIP in h…

0301 basic medicineLiver CirrhosisTime FactorsPhysiologyCASP8 and FADD-Like Apoptosis Regulating ProteinInflammationApoptosisp38 Mitogen-Activated Protein KinasesHepatitisBile Acids and Salts03 medical and health sciencesNecrosisCholestasisPhysiology (medical)medicineHepatic Stellate CellsAnimalsASK1Genetic Predisposition to DiseaseLigationCells CulturedTumor Necrosis Factor alpha-Induced Protein 3chemistry.chemical_classificationLiver injuryCommon Bile DuctMice KnockoutReactive oxygen speciesHepatologyBile duct ligationGastroenterologyTranscription Factor RelAmedicine.diseaseOxidative Stress030104 developmental biologyCholedocholithiasisPhenotypechemistryLiverNeutrophil InfiltrationApoptosisFLICE Inhibitory ProteinCancer researchHepatocytesCytokinesmedicine.symptomInflammation MediatorsSignal TransductionAmerican journal of physiology. Gastrointestinal and liver physiology
researchProduct

Plasma phospholipid transfer protein (PLTP) modulates adaptive immune functions through alternation of T helper cell polarization

2016

International audience; Objective: Plasma phospholipid transfer protein (PLTP) is a key determinant of lipoprotein metabolism, and both animal and human studies converge to indicate that PLTP promotes atherogenesis and its thromboembolic complications. Moreover, it has recently been reported that PLTP modulates inflammation and immune responses. Although earlier studies from our group demonstrated that PLTP can modify macrophage activation, the implication of PLTP in the modulation of T-cell-mediated immune responses has never been investigated and was therefore addressed in the present study. Approach and results: In the present study, we demonstrated that PLTP deficiency in mice has a pro…

0301 basic medicineLymphocyteIpid Transfer ProteinAdaptive ImmunityCardiovascular-DiseaseT-Lymphocytes RegulatoryLipoprotein MetabolismLeukocyte CountPhospholipid transfer proteinPolarizationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyHypersensitivity DelayedPhospholipid Transfer ProteinsCell PolarityCell DifferentiationT-Lymphocytes Helper-InducerT helper cellFlow CytometryAcquired immune systemCell biologyInfectious Diseasesmedicine.anatomical_structureEndothelial-CellsCytokines[SDV.IMM]Life Sciences [q-bio]/ImmunologyLymphocytemedicine.symptomResearch ArticleDensity-Lipoprotein[SDV.IMM] Life Sciences [q-bio]/ImmunologyHuman Atherosclerotic PlaquesT cellCirculating Interleukin-18ImmunologyT CellAntigen-Presenting CellsInflammationAcute Myocardial-InfarctionGATA3 Transcription FactorBiology03 medical and health sciencesImmune systemmedicineAnimalsAntigen-presenting cellDeficient MiceAlpha-TocopherolMice Inbred C57BL030104 developmental biologyImmunologyVitamin-ET-Box Domain ProteinsBiomarkersSpleen
researchProduct

The Role of ERK Signaling in Experimental Autoimmune Encephalomyelitis

2017

Extracellular signal-regulated kinase (ERK) signaling plays a crucial role in regulating immune cell function and has been implicated in autoimmune disorders. To date, all commercially available inhibitors of ERK target upstream components, such as mitogen-activated protein (MAP) kinase/ERK kinase (MEKs), but not ERK itself. Here, we directly inhibit nuclear ERK translocation by a novel pharmacological approach (Glu-Pro-Glu (EPE) peptide), leading to an increase in cytosolic ERK phosphorylation during T helper (Th)17 cell differentiation. This was accompanied by diminished secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine influencing the encephalitogenicity …

0301 basic medicineMAPK/ERK pathwaymedicine.medical_treatmentCellular differentiationexperimental autoimmune encephalomyelitisLymphocyte Activationmedicine.disease_causemultiple sclerosisAutoimmunitylcsh:ChemistryMice0302 clinical medicineT-Lymphocyte SubsetsPhosphorylationExtracellular Signal-Regulated MAP Kinaseslcsh:QH301-705.5SpectroscopyKinaseExperimental autoimmune encephalomyelitisInterleukinGeneral MedicineComputer Science ApplicationsCell biologyProtein TransportCytokine030220 oncology & carcinogenesisFemaleERK pathwayCell signalingEncephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemT cellsBiologyModels BiologicalArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalscell signalingPhysical and Theoretical ChemistryEPE peptideMolecular BiologyT cells; ERK pathway; EPE peptide; experimental autoimmune encephalomyelitis; multiple sclerosis; cell signalingOrganic ChemistryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Th17 CellsInternational Journal of Molecular Sciences
researchProduct

Neutrophils restrain allergic airway inflammation by limiting ILC2 function and monocyte-dendritic cell antigen presentation

2019

Neutrophil mobilization, recruitment, and clearance must be tightly regulated as overexuberant neutrophilic inflammation is implicated in the pathology of chronic diseases, including asthma. Efforts to target neutrophils therapeutically have failed to consider their pleiotropic functions and the implications of disrupting fundamental regulatory pathways that govern their turnover during homeostasis and inflammation. Using the house dust mite (HDM) model of allergic airway disease, we demonstrate that neutrophil depletion unexpectedly resulted in exacerbated T helper 2 (TH2) inflammation, epithelial remodeling, and airway resistance. Mechanistically, this was attributable to a marked increas…

0301 basic medicineMONOCLONAL-ANTIBODYNeutrophilsmedicine.medical_treatmentImmunologyAntigen presentationINNATE LYMPHOID-CELLSInflammationG-CSFGranulocyteArticleMonocytesAllergic sensitizationDOUBLE-BLINDMice03 medical and health sciences0302 clinical medicineSPUTUMHypersensitivitymedicineAnimalsHumansLymphocytesInflammationAntigen PresentationMice Inbred BALB CScience & Technologybusiness.industryMonocyteInnate lymphoid cellDendritic CellsGeneral MedicineDendritic cellCOLONY-STIMULATING FACTORImmunity Innate3. Good health030104 developmental biologymedicine.anatomical_structureCytokineCXCR2 ANTAGONIST AZD5069030228 respiratory systemImmunologyT-CELLSFemalemedicine.symptombusinessLife Sciences & BiomedicineGRANULOCYTESEVERE ASTHMA
researchProduct

Effects of Ranolazine on Astrocytes and Neurons in Primary Culture.

2016

Ranolazine (Rn) is an antianginal agent used for the treatment of chronic angina pectoris when angina is not adequately controlled by other drugs. Rn also acts in the central nervous system and it has been proposed for the treatment of pain and epileptic disorders. Under the hypothesis that ranolazine could act as a neuroprotective drug, we studied its effects on astrocytes and neurons in primary culture. We incubated rat astrocytes and neurons in primary cultures for 24 hours with Rn (10-7, 10-6 and 10-5 M). Cell viability and proliferation were measured using trypan blue exclusion assay, MTT conversion assay and LDH release assay. Apoptosis was determined by Caspase 3 activity assay. The …

0301 basic medicineMacroglial CellsPhysiologyInterleukin-1betaProtein ExpressionCell Culture Techniqueslcsh:MedicineApoptosisPharmacologyPathology and Laboratory Medicine0302 clinical medicineRanolazineAnimal CellsImmune PhysiologyMedicine and Health SciencesEnzyme assaysColorimetric assaysEnzyme-Linked Immunoassayslcsh:ScienceBioassays and physiological analysisImmune ResponseNeuronsInnate Immune SystemMultidisciplinaryMTT assayCell DeathCaspase 3medicine.anatomical_structureCell ProcessesCytokinesTumor necrosis factor alphaCellular TypesAstrocyteResearch ArticleProgrammed cell deathCell SurvivalImmunologyCaspase 3Glial CellsBiologyGene Expression Regulation EnzymologicMitochondrial Proteins03 medical and health sciencesSigns and SymptomsmedicineGene Expression and Vector TechniquesAnimalsMTT assayViability assayMolecular Biology TechniquesImmunoassaysMolecular BiologyInflammationMolecular Biology Assays and Analysis TechniquesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RBiology and Life SciencesCell BiologyMolecular DevelopmentRatsPPAR gammaResearch and analysis methodsOxidative Stress030104 developmental biologyCell cultureApoptosisAstrocytesImmune SystemBiochemical analysisImmunologic Techniqueslcsh:QFisiologia humanaApoptosis Regulatory ProteinsCarrier Proteins030217 neurology & neurosurgeryDevelopmental BiologyPloS one
researchProduct

Gut inflammation in spondyloarthritis

2017

Abstract Spondyloarthritis (SpA) is a group of related diseases sharing common etiopathogenic mechanisms and clinical manifestations supported by a complex genetic predisposition. Gut inflammation is present in patients with SpA including patients showing clinically evident intestinal inflammation in the form of Crohn's disease or ulcerative colitis and patients who despite the absence of signs and symptoms of intestinal inflammation display a subclinical gut inflammation. Emerging evidence suggests that subclinical gut inflammation in patients with SpA, apparently driven by intestinal dysbiosis, is not the consequence of the systemic inflammatory process but rather an important pathophysio…

0301 basic medicineMacrophageSpondyloarthropathyInflammationSystemic inflammationPathogenesis03 medical and health sciences0302 clinical medicineRheumatologySpondylarthritismedicineHumansInnate lymphoid cellCytokineGut inflammationSubclinical infection030203 arthritis & rheumatologyInnate immunityInflammationAnkylosing spondylitisbusiness.industryInnate lymphoid cellPsoriatic arthritimedicine.diseaseUlcerative colitisDysbiosiGastrointestinal MicrobiomeIntestineIntestinesAnkylosing spondylitiSettore MED/16 - Reumatologia030104 developmental biologyImmunologymedicine.symptombusinessDysbiosisHuman
researchProduct

p38α regulates actin cytoskeleton and cytokinesis in hepatocytes during development and aging.

2017

[Background]: Hepatocyte poliploidization is an age-dependent process, being cytokinesis failure the main mechanism of polyploid hepatocyte formation. Our aim was to study the role of p38α MAPK in the regulation of actin cytoskeleton and cytokinesis in hepatocytes during development and aging. [Methods]: Wild type and p38α liver-specific knock out mice at different ages (after weaning, adults and old) were used. [Results]: We show that p38α MAPK deficiency induces actin disassembly upon aging and also cytokinesis failure leading to enhanced binucleation. Although the steady state levels of cyclin D1 in wild type and p38α knock out old livers remained unaffected, cyclin B1- a marker for G2/M…

0301 basic medicineMaleAgingRHOAPhysiologylcsh:MedicineArp2/3 complexBiochemistryMitogen-Activated Protein Kinase 14Gene Knockout TechniquesMice0302 clinical medicineContractile ProteinsAnimal CellsMedicine and Health SciencesSmall interfering RNAsCell Cycle and Cell DivisionPost-Translational ModificationPhosphorylationlcsh:ScienceCytoskeletonCyclin B1Cells CulturedCellular SenescenceCytoskeletonMice KnockoutMultidisciplinarybiologyChemistryImmunohistochemistry3. Good healthCell biologyNucleic acidsLiverCell Processes030220 oncology & carcinogenesisCellular TypesAnatomyCellular Structures and OrganellesProtein BindingResearch ArticleMitosismacromolecular substancesProtein Serine-Threonine Kinases03 medical and health sciencesHsp27CyclinsGeneticsAnimalsNon-coding RNAActinCytokinesislcsh:RBiology and Life SciencesProteinsCell BiologyActin cytoskeletonActinsGene regulationCytoskeletal Proteins030104 developmental biologybiology.proteinHepatocytesRNAlcsh:QGene expressionProtein MultimerizationPhysiological ProcessesOrganism DevelopmentCytokinesisBiomarkersDevelopmental BiologyPloS one
researchProduct

NAFLD and Atherosclerosis Are Prevented by a Natural Dietary Supplement Containing Curcumin, Silymarin, Guggul, Chlorogenic Acid and Inulin in Mice F…

2017

Non-alcoholic fatty liver disease (NAFLD) confers an increased risk of cardiovascular diseases. NAFDL is associated with atherogenic dyslipidemia, inflammation and renin-angiotensin system (RAS) imbalance, which in turn lead to atherosclerotic lesions. In the present study, the impact of a natural dietary supplement (NDS) containing Curcuma longa, silymarin, guggul, chlorogenic acid and inulin on NAFLD and atherosclerosis was evaluated, and the mechanism of action was examined. C57BL/6 mice were fed an HFD for 16 weeks; half of the mice were simultaneously treated with a daily oral administration (os) of the NDS. NAFLD and atherogenic lesions in aorta and carotid artery (histological analys…

0301 basic medicineMaleAngiotensinogenAdministration OralSettore BIO/09 - Fisiologiachemistry.chemical_compoundMice0302 clinical medicineNon-alcoholic Fatty Liver DiseasePlant GumsCommiphorachemistry.chemical_classificationNutrition and Dieteticsnon-alcoholic fatty liver disease; atherogenic lesions; diet-induced obesity; natural dietary supplement; renin-angiotensin system imbalance; Profiler PCR arrayAngiotensin IIFatty liverInulinNeoplasm Proteinsrenin-angiotensin system imbalance030211 gastroenterology & hepatologyatherogenic lesionmedicine.symptomChlorogenic AcidSilymarinmedicine.medical_specialtynatural dietary supplementCurcumindiet-induced obesityProfiler PCR array; atherogenic lesions; diet-induced obesity; natural dietary supplement; non-alcoholic fatty liver disease; renin-angiotensin system imbalanceInflammationBiologyDiet High-FatFatty Acid-Binding ProteinsArticle03 medical and health sciencesInternal medicineRenin–angiotensin systemmedicineAnimalsRNA MessengerProfiler PCR arrayatherogenic lesionsPlant ExtractsFatty acidLipid metabolismmedicine.diseaseAtherosclerosisLipid MetabolismMice Inbred C57BL030104 developmental biologyEndocrinologychemistryGene Expression RegulationSuppressor of Cytokine Signaling 3 ProteinDietary SupplementsCurcuminSteatosisDyslipidemiaFood ScienceNutrients
researchProduct

Venlafaxine prevents morphine antinociceptive tolerance: The role of neuroinflammation and the l-arginine-nitric oxide pathway.

2017

Abstract Opioid-induced neuroinflammation and the nitric oxide (NO) signal-transduction pathway are involved in the development of opioid analgesic tolerance. The antidepressant venlafaxine (VLF) modulates NO in nervous tissues, and so we investigated its effect on induced tolerance to morphine, neuroinflammation, and oxidative stress in mice. Tolerance to the analgesic effects of morphine were induced by injecting mice with morphine (50 mg/kg) once a day for three consecutive days; the effect of co-administration of VLF (5 or 40 mg/kg) with morphine was similarly tested in a separate group. To determine if the NO precursor l -arginine hydrochloride ( l -arg) or NO are involved in the effec…

0301 basic medicineMaleArginineAnalgesicPharmacologymedicine.disease_causeNitric oxideProinflammatory cytokine03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineDevelopmental NeurosciencemedicineAnimalsEnzyme InhibitorsNitritesPain Measurementchemistry.chemical_classificationGlutathione PeroxidaseDose-Response Relationship DrugMorphineGlutathione peroxidaseVenlafaxine HydrochlorideBrainMalondialdehydeAnalgesics OpioidDisease Models AnimalOxidative Stress030104 developmental biologyNG-Nitroarginine Methyl EsterNeurologychemistryMorphineAntidepressive Agents Second-GenerationCytokinesLipid PeroxidationMorphine Dependence030217 neurology & neurosurgeryOxidative stressmedicine.drugSignal TransductionExperimental neurology
researchProduct