Search results for " cytokine"

showing 10 items of 602 documents

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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Lung CD11c+ cells from mice deficient in Epstein-Barr virus-induced gene 3 (EBI-3) prevent airway hyper-responsiveness in experimental asthma

2007

Epstein-Barr virus-induced gene (EBI)-3 codes for a soluble type 1 cytokine receptor homologous to the p40 subunit of IL-12 that is expressed by antigen-presenting cells following activation. Here, we analyzed the functional role of EBI-3 in a murine model of asthma associated with airway hyper-responsiveness (AHR) in ovalbumin-sensitized mice. Upon allergen challenge, EBI-3-/- mice showed less severe AHR, decreased numbers and degranulation of eosinophils and a significantly reduced number of VCAM-1+ cells in the lungs as compared to wild-type littermates. We thus analyzed lung CD11c+ cells before and after allergen challenge in these mice and found that before allergen challenge, lung CD1…

Adoptive cell transferMyeloidCell TransplantationImmunologyVascular Cell Adhesion Molecule-1CD11cCD8-Positive T-LymphocytesBiologyMinor Histocompatibility AntigensInterferon-gammaMiceImmune systemmedicineAnimalsImmunology and AllergyReceptors CytokineLungCell ProliferationMice KnockoutLungTumor Necrosis Factor-alphaEffectorDegranulationInterferon-alphaDendritic CellsSTAT4 Transcription Factorrespiratory systemInterleukin-12AsthmaCD11c AntigenInterleukin-10respiratory tract diseasesEosinophilsMice Inbred C57BLmedicine.anatomical_structureImmunologyInterleukin-4Bronchial HyperreactivityInterleukin-5T-Box Domain ProteinsCytokine receptorBronchoalveolar Lavage FluidEuropean Journal of Immunology
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Liver-specific p38α deficiency causes reduced cell growth and cytokinesis failure during chronic biliary cirrhosis in mice

2012

p38α mitogen-activated protein kinases (MAPK) may be essential in the up-regulation of proinflammatory cytokines and can be activated by transforming growth factor β, tumor necrosis factor-α, interleukin-1β, and oxidative stress. p38 MAPK activation results in hepatocyte growth arrest, whereas increased proliferation has been considered a hallmark of p38α-deficient cells. Our aim was to assess the role of p38α in the progression of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflammation associated with hepatocyte proliferation, apoptosis, oxidative stress, and fibrogenesis. Cholestasis was induced in wildtype and liver-specific p38α knockout mice by…

Malemedicine.medical_specialtyBiliary cirrhosisMAP Kinase Kinase 2ApoptosisBiologymedicine.disease_causeProinflammatory cytokineMitogen-Activated Protein Kinase 14MiceCholestasisInternal medicinemedicineAnimalsCyclin D1Cyclin B1Cell ProliferationCytokinesisMice KnockoutHepatologyLiver Cirrhosis BiliaryHepatologymedicine.diseaseMice Inbred C57BLSurvival RateDisease Models AnimalOxidative Stressmedicine.anatomical_structureEndocrinologyLiverHepatocyteChronic DiseaseDisease ProgressionHepatocytesTumor necrosis factor alphaOxidative stressSignal TransductionTransforming growth factorHepatology
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Nivolumab Enhances In Vitro Effector Functions of PD-1+ T-Lymphocytes and Leishmania-Infected Human Myeloid Cells in a Host Cell-Dependent Manner

2017

Functional impairment of T-cells and a concomitant augmented expression of programmed death-1 (PD-1) have been observed in visceral leishmaniasis patients, as well as in experimental models for visceral and cutaneous leishmaniasis. The PD-1/PD-1-ligand (PD-1/PD-L) interaction negatively regulates T-cell effector functions, which are required for parasite control during leishmaniasis. The aim of this study was to elucidate the impact of the PD-1/PD-L axis in a human primary in vitro infection model of Leishmania major (Lm). Blocking the PD-1/PD-L interaction with nivolumab increased T-cell proliferation and release of the proinflammatory cytokines TNFα and IFNγ during the cocultivation of Lm…

lcsh:Immunologic diseases. Allergyprogrammed death-1 ligand 10301 basic medicineprogrammed death-1 ligand 2ImmunologyProinflammatory cytokine03 medical and health sciencesCutaneous leishmaniasisPD-L1medicineImmunology and AllergyLeishmania majorGranulysinOriginal Researchprogrammed death-1Leishmanianivolumabhuman macrophagesbiologyT-cellsmedicine.diseasebiology.organism_classification030104 developmental biologyGranzymePerforinImmunologybiology.proteinTumor necrosis factor alphahuman dendritic cellslcsh:RC581-607Frontiers in Immunology
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Lipoxygenase-derived arachidonic acid metabolites in chronic obstructive pulmonary disease

2011

Background and Objective. Chronic obstructive pulmonary disease (COPD) is characterized by a persistence of inflammation in large and small airways. We hypothesized that this could be caused by the inability of an inflammatory process to resolve. In the resolution of inflammation, a switching of arachidonic acid metabolism from the production of proinflammatory leukotriene B4 (LtB4) to the synthesis of anti-inflammatory lipoxins plays an important role. The aim of our study was to determine the content of lipoxin A4 (LXA4) and LtB4 in induced sputum of patients with exacerbated COPD and to compare it to healthy controls, as well as to analyze the relationship between proinflammatory and ant…

MaleSputum CytologyExacerbationLeukotriene B4InflammationLeukotriene B4Proinflammatory cytokinePulmonary Disease Chronic Obstructivechemistry.chemical_compoundHumansMedicineCOPDbusiness.industrySputumGeneral MedicineMiddle Agedmedicine.diseaserespiratory tract diseasesLipoxinschemistrychronic obstructive pulmonary disease; exacerbation; lipoxin A<sub>4</sub>; leukotriene B<sub>4</sub>ImmunologyAbsolute neutrophil countSputumFemalelipids (amino acids peptides and proteins)medicine.symptombusiness
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FTY720 reduces post-ischemic brain lymphocyte influx but does not improve outcome in permanent murine cerebral ischemia.

2011

Background The contribution of neuroinflammation and specifically brain lymphocyte invasion is increasingly recognised as a substantial pathophysiological mechanism after stroke. FTY720 is a potent treatment for primary neuroinflammatory diseases by inhibiting lymphocyte circulation and brain immigration. Previous studies using transient focal ischemia models showed a protective effect of FTY720 but did only partially characterize the involved pathways. We tested the neuroprotective properties of FTY720 in permanent and transient cortical ischemia and analyzed the underlying neuroimmunological mechanisms. Methodology/Principal Findings FTY720 treatment resulted in substantial reduction of c…

MaleDrugs and DevicesLymphocyteCerebrovascular DiseasesImmunologyNeuroimmunologyIschemialcsh:MedicineBrain EdemaNeuroprotectionProinflammatory cytokineBrain IschemiaBrain ischemiaMiceNeuropharmacologySphingosinemedicine.arteryhemic and lymphatic diseasesmedicineLeukocytesAnimalsLymphoid OrgansLymphocyteslcsh:ScienceStrokeBiologyNeuroinflammationMultidisciplinarybusiness.industryFingolimod HydrochlorideInterleukin-6Tumor Necrosis Factor-alphalcsh:RImmunologic Subspecialtiesmedicine.diseaseMice Inbred C57BLmedicine.anatomical_structureNeurologyPropylene GlycolsImmune SystemImmunologyMiddle cerebral arteryMedicineClinical Immunologylcsh:QbusinessImmunosuppressive AgentsResearch ArticlePLoS ONE
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Pathophysiology of polymorphonuclear leukocyte in arterial hypertension

2009

This review shows how polymorphonuclear leukocytes (PMNs) play a pivotal role in the development of the organ injury that is associated with arterial hypertension. Elevated white blood cell count and higher levels of PMNs activation are risk factors for arterial hypertension and cardiovascular disease. Spontaneously activated PMNs release proinflammatory factors and reactive oxygen species, which have negative effects on vascular tone and on their adhesion to the endothelium. The oxidative stress in hypertensive PMNs is revealed by increased NADPH-oxidase production and lipid peroxidation and by decreased cytosolic and mitochondrial superoxide dismutase concentrations. The overexpression of…

medicine.medical_specialtyEndotheliumNeutrophilsPhysiologyPolymorphonuclear leukocyte Hypertension oxidative stress adhesion moleculesmedicine.disease_causeProinflammatory cytokineSuperoxide dismutaseLipid peroxidationLeukocyte Countchemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansLeukocyte Rollingchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxide Dismutasebusiness.industryCell adhesion moleculeNADPH OxidasesHematologymedicine.anatomical_structureEndocrinologychemistryCD18 AntigensHypertensionImmunologybiology.proteinLipid PeroxidationCardiology and Cardiovascular MedicinebusinessOxidative stressClinical Hemorheology and Microcirculation
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A non-redundant role for OX40 in the competitive fitness of Treg in response to IL-2.

2010

OX40 stimulation is known to enhance activation of effector T cells and to inhibit induction and suppressive function of Treg. Here we uncovered a novel role of OX40 in sustaining Treg competitive fitness in vivo, during repopulation of lymphopenic hosts and reconstitution of BM chimeras. Defective expansion of OX40-null Treg diminished their ability to suppress inflammation in a model of lymphopenia-driven colitis. OX40-mediated promotion of Treg fitness spanned beyond lymphopenic environments, as endogenous Treg in OX40-null mice showed decreased accumulation during thymic development, enhanced susceptibility to antibody-mediated depletion and defective turnover following thymectomy. In v…

Malemedicine.medical_treatmentImmunologyBlotting Westernchemical and pharmacologic phenomenaEndogenyInflammationSuppressor of Cytokine Signaling ProteinsT-Lymphocytes RegulatoryMiceSuppressor of Cytokine Signaling 1 ProteinLymphopeniaOX40; Treg; IL-2.medicineSTAT5 Transcription FactorImmunology and AllergyAnimalsOX40PhosphorylationReceptorSTAT5Cell ProliferationMice KnockoutbiologyEffectorCell growthSuppressor of cytokine signaling 1hemic and immune systemsReceptors OX40IL-2.ColitisFlow Cytometrycytokinescompetitive fitnessSpecific Pathogen-Free OrganismsThymectomyMice Inbred C57BLTregRadiation ChimeraImmunologybiology.proteinInterleukin-2costimulatory moleculesmedicine.symptomcompetitive fitness; costimulatory molecules; cytokines; treg
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Exposure to ototoxic agents and hearing loss: A review of current knowledge

2014

Several experimental and clinical studies have shown that a variety of ototoxic agents (such as drugs, industrial chemicals and noise) can cause sensorineural hearing loss. The most common ototoxic drugs used in clinical practice include: aminoglycoside and macrolide antibiotics, quinoline anti-malarials, platinum analog antineoplastics, loop diuretics, and acetylsalicylic acid. Among chemical agents with potential ototoxic properties are: organic solvents, heavy metals, organotins, nitriles, asphyxiants, and pesticides/herbicides. Acoustic exposure to high intensity and/or prolonged noise can also cause permanent threshold shifts in auditory perception. Ototoxic agents can influence audito…

medicine.medical_specialtypharmacological injuryEndolymphHearing lossototoxicity hearing loss pharmacological injury reactive oxygen speciesPharmacologyAudiologyProinflammatory cytokineSpeech and HearingAtrophyOtotoxicitymedicinehearing lossreactive oxygen specieschemistry.chemical_classificationReactive oxygen speciesbusiness.industrySettore MED/44 - Medicina Del LavoroAminoglycosidemedicine.diseaseototoxicity; hearing loss; pharmacological injury; reactive oxygen speciesSettore MED/32 - AudiologiaototoxicitySettore MED/31 - Otorinolaringoiatriamedicine.anatomical_structureOtorhinolaryngologychemistrySettore BIO/14 - FarmacologiaSensorineural hearing lossmedicine.symptombusinessHearing, Balance and Communication
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Tissue factor pathway inhibitor primes monocytes for antiphospholipid antibody-induced thrombosis

2019

Antiphospholipid antibodies (aPLs) with complex lipid and/or protein reactivities cause complement-dependent thrombosis and pregnancy complications. Although cross-reactivities with coagulation regulatory proteins contribute to the risk for developing thrombosis in patients with antiphospholipid syndrome, the majority of pathogenic aPLs retain reactivity with membrane lipid components and rapidly induce reactive oxygen species-dependent proinflammatory signaling and tissue factor (TF) procoagulant activation. Here, we show that lipid-reactive aPLs activate a common species-conserved TF signaling pathway. aPLs dissociate an inhibited TF coagulation initiation complex on the cell surface of m…

Male0301 basic medicineLipoproteinsImmunologyPlenary Paper030204 cardiovascular system & hematologyBiochemistryMonocytesThromboplastinProinflammatory cytokine03 medical and health sciencesTissue factor0302 clinical medicineTissue factor pathway inhibitorThrombinimmune system diseasesmedicineAnimalsHumansThromboplastinBlood CoagulationneoplasmsCells CulturedNADPH oxidasebiologyChemistryThrombosisCell BiologyHematologyComplement systemMice Inbred C57BL030104 developmental biologyAntibodies Antiphospholipidbiology.proteinCancer researchFemaleSignal transductionSignal Transductionmedicine.drugBlood
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