Search results for "tumor necrosis factor alpha"

showing 10 items of 479 documents

Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model.

2018

INTRODUCTION:The acute respiratory distress syndrome is not only associated with a high mortality, but also goes along with cognitive impairment in survivors. The cause for this cognitive impairment is still not clear. One possible mechanism could be cerebral inflammation as result of a "lung-brain-crosstalk". Even mechanical ventilation itself can induce cerebral inflammation. We hypothesized, that an acute lung injury aggravates the cerebral inflammation induced by mechanical ventilation itself and leads to neuronal damage. METHODS:After approval of the institutional and state animal care committee 20 pigs were randomized to one of three groups: lung injury by central venous injection of …

MaleARDSCritical Care and Emergency MedicinePulmonologySwinePhysiologymedicine.medical_treatmentVentilator-Induced Lung InjuryInterleukin-1betalcsh:MedicineApoptosisPathology and Laboratory MedicineHippocampusPositive-Pressure RespirationRandom Allocation0302 clinical medicineAnimal CellsImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseAcute Respiratory Distress SyndromeTidal volumeCerebral CortexNeuronsCognitive ImpairmentRespiratory Distress SyndromeInnate Immune SystemMultidisciplinarymedicine.diagnostic_testCognitive NeurologyBrainGeneral MedicineLung InjuryNeurologyAnesthesiaBreathingCytokinesTumor necrosis factor alphamedicine.symptomAnatomyCellular TypesGeneral Agricultural and Biological SciencesResearch ArticleHistologyCognitive NeuroscienceImmunology10208 Institute of NeuropathologyInflammation610 Medicine & healthGenetics and Molecular BiologyGlial Cells1100 General Agricultural and Biological SciencesLung injury03 medical and health sciencesSigns and SymptomsRespiratory Failure1300 General Biochemistry Genetics and Molecular BiologyDiagnostic MedicinemedicineAnimalsMicroglial CellsMechanical ventilationInflammation1000 Multidisciplinarybusiness.industryInterleukin-6Tumor Necrosis Factor-alphalcsh:RBiology and Life Sciences030208 emergency & critical care medicineCell BiologyMolecular Developmentmedicine.diseaseRespiration ArtificialBronchoalveolar lavage030228 respiratory systemImmune SystemCellular NeuroscienceGeneral Biochemistry570 Life sciences; biologyCognitive Sciencelcsh:QbusinessDevelopmental BiologyNeurosciencePloS one
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Apremilast, a novel phosphodiesterase 4 (PDE4) inhibitor, regulates inflammation through multiple cAMP downstream effectors

2015

Introduction This work was undertaken to delineate intracellular signaling pathways for the PDE4 inhibitor apremilast and to examine interactions between apremilast, methotrexate and adenosine A2A receptors (A2AR). Methods After apremilast and LPS incubation, intracellular cAMP, TNF-α, IL-10, IL-6 and IL-1α were measured in the Raw264.7 monocytic murine cell line. PKA, Epac1/2 (signaling intermediates for cAMP) and A2AR knockdowns were performed by shRNA transfection and interactions with A2AR and A2BR, as well as with methotrexate were tested in vitro and in the murine air pouch model. Statistical differences were determined using one or two-way ANOVA or Student’s t test. The alpha nominal…

MaleAdenosineReceptor Adenosine A2AImmunologyBlotting WesternAdenosine A2A receptorGene ExpressionPharmacologyBiologyCell LineMiceRheumatologyPhenethylaminesmedicineCyclic AMPImmunology and AllergyAnimalsGuanine Nucleotide Exchange FactorsReceptorIC50ArtritisReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaMacrophagesAdenosineMolecular biologyCyclic AMP-Dependent Protein KinasesThalidomideMethotrexateMechanism of actionAntirheumatic AgentsCytokinesTumor necrosis factor alphaRNA InterferenceApremilastPhosphodiesterase 4 Inhibitorsmedicine.symptomInflammation MediatorsIntracellularMedicamentsmedicine.drugResearch Article
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Analysis of early biochemical markers and regulation by tin protoporphyrin IX in a model of spontaneous osteoarthritis

2011

Abstract Age-related changes in joint tissues lead to osteoarthritis (OA). Detection of early changes in OA patients may help to initiate treatments before the establishment of irreversible joint destruction. STR/ort mice develop with age a severe degenerative joint disease that resembles human OA thus allowing the investigation of biochemical markers as well as new treatments in an accelerated time frame. We have analyzed the changes in serum levels of different mediators during the early phases of idiopathic OA in STR/ort mice. Serum levels of matrix metalloproteinase-3 (MMP-3) but not those of tumor necrosis factor-α, interleukin(IL)-1β, IL-17 or prostaglandin E 2 correlated with histopa…

MaleAgingmedicine.medical_specialtyPathologyMetalloporphyrinsmedicine.medical_treatmentDrug Evaluation PreclinicalProtoporphyrinsMice Inbred StrainsOsteoarthritisMatrix metalloproteinaseBiochemistryMiceEndocrinologyInternal medicineOsteoarthritisGeneticsmedicineAnimalsEnzyme InhibitorsMolecular BiologyBiochemical markersbusiness.industryInterleukinCell BiologyClinical Enzyme TestsTin protoporphyrin IXmedicine.diseaseArthritis ExperimentalEarly DiagnosisEndocrinologyHeme Oxygenase (Decyclizing)Disease ProgressionBiomarker (medicine)Matrix Metalloproteinase 3Tumor necrosis factor alphaInflammation MediatorsbusinessBiomarkersProstaglandin EExperimental Gerontology
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In activated mast cells, IL-1 up-regulates the production of several Th2-related cytokines including IL-9.

2000

Abstract Mast cells can play detrimental roles in the pathophysiology and mortality observed in anaphylaxis and other Th2-dominated allergic diseases. In contrast, these cells contribute to protective host defense mechanisms against parasitic worm infections. After IgE/Ag activation, mast cells can produce multiple cytokines that may enhance allergic inflammations, while a similar panel of Th2-related cytokines may support immunological strategies against parasites. Here we report that in primary mouse bone marrow-derived mast cells activated by ionomycin or IgE/Ag, the proinflammatory mediator IL-1 (α or β) up-regulated production of IL-3, IL-5, IL-6, and IL-9 as well as TNF, i.e., cytokin…

MaleAllergymedicine.medical_treatmentImmunologyDose-Response Relationship ImmunologicInflammationBone Marrow CellsBiologyImmunoglobulin EProinflammatory cytokineImmunophenotypingchemistry.chemical_compoundMiceTh2 CellsAdjuvants ImmunologicmedicineImmunology and AllergyAnimalsMast CellsRNA MessengerMice Inbred BALB CIonomycinInterleukin-9Cell DifferentiationSerum Albumin BovineImmunoglobulin Emedicine.diseaseUp-RegulationInterleukin 33Autocrine CommunicationKineticsCytokinechemistryIonomycinImmunologybiology.proteinCytokinesTumor necrosis factor alphaFemaleInterleukin-4medicine.symptomDinitrophenolsInterleukin-1Journal of immunology (Baltimore, Md. : 1950)
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Incidence, Clinical Characteristics, and Management of Psoriasis Induced by Anti-TNF Therapy in Patients with Inflammatory Bowel Disease: A Nationwid…

2016

Background: Psoriasis induced by anti-tumor necrosis factor-alpha (TNF) therapy has been described as a paradoxical side effect. Aim: To determine the incidence, clinical characteristics, and management of psoriasis induced by anti-TNF therapy in a large nationwide cohort of inflammatory bowel disease patients. Methods: Patients with inflammatory bowel disease were identified from the Spanish prospectively maintained Estudio Nacional en Enfermedad Inflamatoria Intestinal sobre Determinantes geneticos y Ambientales registry of Grupo Espanol de Trabajo en Enfermedad de Croh y Colitis Ulcerosa. Patients who developed psoriasis by anti-TNF drugs were the cases, whereas patients treated with ant…

MaleAnti-Inflammatory AgentsInflammatory bowel diseaseGastroenterologyCohort Studies030207 dermatology & venereal diseases0302 clinical medicineCrohn DiseaseadalimumabImmunology and AllergyIncidence (epidemiology)IncidenceGastroenterologypsoriasisPrognosisside effectsCrohn's diseaseCohort030211 gastroenterology & hepatologyTumor necrosis factor alphaFemaleCohort studyAdultmedicine.medical_specialtyAdolescent03 medical and health sciencesGastrointestinal Agentsinflammatory bowel diseasePsoriasisInternal medicinemedicineHumansPsoriasisColitisulcerative colitisbusiness.industryTumor Necrosis Factor-alphaCase-control studyAdalimumabanti-TNFmedicine.diseaseInfliximabWithholding TreatmentSpainCase-Control StudiesPhysical therapyColitis UlcerativebusinessinfliximabFollow-Up Studies
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Janus -faced liposomes enhance antimicrobial innate immune response in Mycobacterium tuberculosis infection

2012

We have generated unique asymmetric liposomes with phosphatidylserine (PS) distributed at the outer membrane surface to resemble apoptotic bodies and phosphatidic acid (PA) at the inner layer as a strategy to enhance innate antimycobacterial activity in phagocytes while limiting the inflammatory response. Results show that these apoptotic body-like liposomes carrying PA (ABL/PA) ( i ) are more efficiently internalized by human macrophages than by nonprofessional phagocytes, ( ii ) induce cytosolic Ca 2+ influx, ( iii ) promote Ca 2+ -dependent maturation of phagolysosomes containing Mycobacterium tuberculosis (MTB), ( iv ) induce Ca 2+ -dependent reactive oxygen species (ROS) production, (…

MaleAntitubercular AgentsApoptosisSettore MED/07Mice0302 clinical medicineInnateInbred BALB CMycobacterium tuberculosis liposomes0303 health sciencesMice Inbred BALB CMultidisciplinaryLeukemiaTumorbiologyMacrophages; Leukemia Monocytic Acute; Animals; Apoptosis; Calcium; Humans; Disease Models Animal; Mice; Cell Line Tumor; Immunity Innate; Reactive Oxygen Species; Mice Inbred BALB C; Liposomes; Phosphatidylserines; Tuberculosis Pulmonary; Adult; Bronchoalveolar Lavage Fluid; Middle Aged; Antitubercular Agents; Phagocytosis; Male; Mycobacterium tuberculosis; IsoniazidInterleukinPulmonaryMiddle AgedSettore BIO/193. Good healthPNAS PlusLeukemia Monocytic AcuteTumor necrosis factor alphaBronchoalveolar Lavage FluidIntracellularAdultPhagocytosisPhosphatidylserinesAcutePhagolysosomeSettore MED/07 - MICROBIOLOGIA E MICROBIOLOGIA CLINICAMicrobiologyCell LineMycobacterium tuberculosis03 medical and health sciencesPhagocytosisCell Line TumorIsoniazidTuberculosisAnimalsHumansTuberculosis Pulmonary030304 developmental biologySettore MED/04 - Patologia GeneraletherapyInnate immune systemMonocyticAnimalMacrophagesImmunityMycobacterium tuberculosisbiology.organism_classificationImmunity InnateDisease Models AnimalApoptosisImmunologyDisease ModelsLiposomesCalciumReactive Oxygen Species030215 immunology
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Tumor necrosis-factor-alpha -308 A/G polymorphism is associated with age at onset of Alzheimer's disease.

2006

Abstract Pro-inflammatory cytokines and acute-phase proteins play an important role in Alzheimer's disease (AD) neurodegeneration, and common polymorphisms of genes controlling their production have been shown to be associated with AD. Tumor necrosis factor (TNF)-α is an inflammatory cytokine involved in the local immune response occurring in the central nervous system of AD patients. Genetic variation could contribute to the risk of developing AD or influence the age at the onset of the disease. We genotyped 222 patients (152 women, 70 men; age range 60–87) and 240 non-demented age-matched healthy controls for TNF-α −308 G/A single nucleotide polymorphism (SNP). No significant differences …

MaleApolipoprotein EAgingGenotypemedicine.medical_treatmentSNPSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideWhite PeopleAlzheimer DiseaseRisk FactorsGenotypecytokinemedicineHumansGenetic Predisposition to DiseaseAge of OnsetAlleleAgedAged 80 and overTumor Necrosis Factor-alphaalzheimer TNF polymorphisms age of onsetMiddle AgedAlzheimer's diseasemedicine.diseaseCytokineItalyinflammationImmunologyFemaleTumor necrosis factor alphaMED/09 - MEDICINA INTERNAAge of onsetAlzheimer's diseaseTNF-alphaDevelopmental Biology
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CD14+CD16+ monocytes in coronary artery disease and their relationship to serum TNF-α levels

2004

SummaryMonocytes play a central role in the inflammatory disease atherosclerosis. CD14+CD16+ monocytes are considered proinflammatory monocytes, as they have an increased capacity to produce proinflammatory cytokines, such as TNF-α, and are elevated in various inflammatory diseases. We hypothesized that patients with coronary artery disease (CAD) have increased levels of CD14+CD16+ monocytes, and that CD14+CD16+ monocytes are associated with inflammation markers. We investigated CD14+CD16+ monocytes in 247 patients with CAD and 61 control subjects using flow cytometry. In addition serum concentrations of TNF-α, IL-6, and Hs-CRP were assessed. Patients with CAD had higher levels of CD14+CD16…

MaleArteriosclerosismedicine.medical_treatmentCD14Lipopolysaccharide ReceptorsInflammationCell SeparationCoronary Artery DiseaseCD16MonocytesBody Mass IndexProinflammatory cytokineCoronary artery diseaseRisk FactorsOdds RatioHumansMedicineAgedInflammationAnalysis of VarianceInterleukin-6Tumor Necrosis Factor-alphabusiness.industryMonocyteReceptors IgGAntibodies MonoclonalHematologyMiddle AgedFlow Cytometrymedicine.diseaseLogistic ModelsCytokinemedicine.anatomical_structureCase-Control StudiesImmunologyFemaleTumor necrosis factor alphamedicine.symptombusinessThrombosis and Haemostasis
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Conditioned Media from Adipose-Tissue-Derived Mesenchymal Stem Cells Downregulate Degradative Mediators Induced by Interleukin-1β in Osteoarthritic C…

2013

Osteoarthritis (OA) is the most frequent joint disorder and an important cause of disability. Recent studies have shown the potential of adipose-tissue-derived mesenchymal stem cells (AD-MSC) for cartilage repair. We have investigated whether conditioned medium from AD-MSC (CM) may regulate in OA chondrocytes a number of key mediators involved in cartilage degeneration. CM enhanced type II collagen expression in OA chondrocytes while decreasing matrix metalloproteinase (MMP) activity in cell supernatants as well as the levels of MMP-3 and MMP-13 proteins and mRNA in OA chondrocytes stimulated with interleukin- (IL-) 1β. In addition, CM increased IL-10 levels and counteracted the stimulating…

MaleArticle Subjectmedicine.medical_treatmentImmunologyInterleukin-1betaType II collagenAdipose tissueDown-RegulationNitric OxideChondrocytesMatrix Metalloproteinase 13Osteoarthritislcsh:PathologymedicineHumansProstaglandin E2Interleukin 6Collagen Type IICells CulturedAgedbiologyChemistryInterleukin-6Tumor Necrosis Factor-alphaMesenchymal stem cellNF-kappa BInterleukinMesenchymal Stem CellsCell BiologyMiddle AgedCell biologyAdipose TissueCulture Media ConditionedImmunologybiology.proteinTumor necrosis factor alphaFemaleMatrix Metalloproteinase 3Inflammation Mediatorslcsh:RB1-214Prostaglandin Emedicine.drugResearch Article
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Effect of autologous blood transfusion on cerebral cytokine expression.

2011

BACKGROUND: Autologous blood transfusion (ABT), for example, by means of cell saver equipment, is used to reduce the need for allogenic blood transfusion in patients with high perioperative blood loss. This study investigated the effect of blood/extracorporal surface interaction during withdrawal and retransfusion of shed autologous blood on cerebral inflammation in rats. Rats subjected to hypotension with cerebral ischemia served as positive controls. METHODS: Eighty-eight male Sprague-Dawley rats were anesthetized with sevoflurane, instrumented, and randomly assigned to the following groups: sham-operation (SHAM), autologous blood withdrawal/transfusion only (ABT), or bilateral carotid ar…

MaleBlood transfusionmedicine.medical_treatmentInterleukin-1betaIschemiaNitric Oxide Synthase Type IIInflammationPharmacologySevofluraneRats Sprague-DawleyBlood Transfusion AutologousmedicineHippocampus (mythology)AnimalsInterleukin 6biologybusiness.industryInterleukin-6Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaBrainmedicine.diseaseRatsNitric oxide synthaseAnesthesiology and Pain MedicineCyclooxygenase 2biology.proteinCytokinesSurgeryTumor necrosis factor alphaNeurology (clinical)medicine.symptombusinessmedicine.drugFollow-Up StudiesJournal of neurosurgical anesthesiology
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