Search results for " interleukin-6"

showing 10 items of 93 documents

Inflammation and sarcopenia: A systematic review and meta-analysis

2017

Inflammatory cytokines have been shown to prompt muscle wasting, ultimately stimulating protein catabolism and suppressing muscle synthesis. However, the possible association between inflammatory parameters and sarcopenia is poorly understood. We therefore aimed to summarize the current evidence about this topic with a meta-analysis of studies reporting serum inflammatory parameters in patients with sarcopenia vs. people without sarcopenia (controls). An electronic PubMed and Scopus search through to 09/01/2016 and meta-analysis of cross-sectional studies comparing serum levels of inflammatory cytokines between patients with sarcopenia and controls was made, calculating random-effects stand…

Sarcopenia Inflammation Meta-analysis C reactive proteinmedicine.medical_specialtySarcopeniaInflammationGastroenterologyGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineNOsarcopenia03 medical and health sciences0302 clinical medicineC reactive protein; Inflammation; Meta-analysis; Sarcopenia; Biomarkers; C-Reactive Protein; Case-Control Studies; Cross-Sectional Studies; Humans; Inflammation; Interleukin-6; Sarcopenia; Tumor Necrosis Factor-alphaInternal medicinemedicineHumans030212 general & internal medicineWastingInflammationC reactive proteinbiologybusiness.industryInterleukin-6Tumor Necrosis Factor-alphaC-reactive proteinObstetrics and Gynecologymedicine.diseaseConfidence intervalmeta-analysisProtein catabolismMeta-analysisEndocrinologyC-Reactive ProteinCross-Sectional StudiesinflammationSarcopeniaMeta-analysisCase-Control Studiesbiology.proteinmedicine.symptombusiness030217 neurology & neurosurgeryBiomarkers
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Significance of Autologous Interleukin-6 Production in the HA22T/VGH Cell Model of Hepatocellular Carcinoma

2006

Cancer cells may often support their own growth, survival, and drug resistance by autocrine/paracrine loops based on the production of different factors; results from us and others have shown that similar interleukin-6 (IL-6)-related loops are operative in multiple myeloma and prostate or renal cancer. Because this aspect has not been investigated in detail for hepatocellular carcinoma (HCC), we have examined it in HA22T/VGH cells. These differ from other primary liver cancer cell lines (that is, HepG2, HuH-6, and HuH-7) in that enzyme-linked immunosorbent assay (ELISA) showed the HA22T/VGH cells to secrete remarkable amounts of IL-6 (16.8 ng/10(6) cells/24 h); this production, due to const…

Settore MED/09 - Medicina InternaCarcinoma HepatocellularCurcuminCellBiologyautocrine cellgrowth stimulatory loopModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyAntibodiesFlow cytometryParacrine signallingHistory and Philosophy of SciencemedicineCytokine Receptor gp130Tumor Cells CulturedHumansNF-kBRNA Small InterferingReceptorAutocrine signallingNF-k Bmedicine.diagnostic_testCyclohexanonesGeneral Neuroscienceinterleukin-6Cell MembraneLiver NeoplasmsNF-kappa Bhepatocellular carcinomaMolecular biologyReceptors Interleukin-6medicine.anatomical_structureCell cultureCancer cellBenzamidesbiology.proteinSettore BIO/14 - Farmacologiaautocrine cell growth stimulatory loopAntibody
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Novel pathogenic mechanism of microbial metalloproteinases: liberation of membrane-anchored molecules in biologically active form exemplified by stud…

1996

Certain membrane-anchored proteins, including several cytokines and cytokine receptors, can be released into cell supernatants through the action of endogenous membrane-bound metalloproteinases. The shed molecules are then able to fulfill various biological functions; for example, soluble interleukin-6 receptor (sIL-6R) can bind to bystander cells, rendering these cells sensitive to the action of IL-6. Using IL-6R as a model substrate, we report that the metalloproteinase from Serratia marcescens mimics the action of the endogenous shedding proteinase. Treatment of human monocytes with the bacterial protease led to a rapid release of sIL-6R into the supernatant. This effect was inhibitable …

Staphylococcus aureusProteasesmedicine.medical_treatmentImmunologyBiologyMatrix metalloproteinaseMicrobiologyMonocytesSubstrate SpecificityAntigens CDChlorocebus aethiopsmedicineAnimalsHumansReceptorSerratia marcescensMetalloproteinaseProteaseMembrane ProteinsMetalloendopeptidasesBiological activityBacterial InfectionsReceptors InterleukinListeria monocytogenesReceptors Interleukin-6Recombinant ProteinsBlotInfectious DiseasesSolubilityBiochemistryPseudomonas aeruginosaParasitologySignal transductionResearch ArticleSignal TransductionInfection and Immunity
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Selective killing of human monocytes and cytokine release provoked by sphingomyelinase (beta-toxin) of Staphylococcus aureus.

1996

The best-known activity of Staphylococcus aureus sphingomyelinase C, alias beta-toxin, is as a hemolysin that provokes hot-cold lysis of erythrocytes which contain substantial amounts of sphingomyelin in the plasma membrane. Sheep erythrocytes are most susceptible, and we found that one hemolytic unit, representing the toxin concentration that elicits 50% hemolysis of 2.5 X 10(8) erythrocytes per ml, corresponds to 0.05 enzyme units or to approximately 0.25 microg of sphingomyelinase per ml. The cytotoxic action of beta-toxin on nucleated cells has not been described in any detail before, and the present investigation was undertaken to fill this information gap. We now identify beta-toxin a…

Staphylococcus aureusTime FactorsLipopolysaccharideCD14ImmunologyBacterial ToxinsLipopolysaccharide ReceptorsExotoxinsMicrobiologyMonocytesMicrobiologychemistry.chemical_compoundHemolysin ProteinsPhospholipase A2Antigens CDmedicineHumansbiologyCell DeathDose-Response Relationship DrugCytotoxinsMonocyteHemolysinReceptors Interleukinmedicine.diseaseReceptors Interleukin-6HemolysisInfectious Diseasesmedicine.anatomical_structureSphingomyelin PhosphodiesteraseMechanism of actionchemistrybiology.proteinCytokinesParasitologymedicine.symptomSphingomyelinResearch ArticleInterleukin-1
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Sympathetic neurons can produce and respond to interleukin 6

1998

Neuronal expression of cytokines is an area of active investigation in the contexts of development, disease, and normal neural function. Although cultured rat sympathetic neurons respond very weakly to exogenous interleukin 6 (IL-6), we find that addition of soluble IL-6 receptor (sIL-6R) and IL-6 enhances neuronal survival in the absence of nerve growth factor. Neutralizing monoclonal antibodies against IL-6 block these effects. Addition of IL-6 and sIL-6R also induces a subset of neuropeptide and transmitter synthetic enzyme mRNAs identical to that demonstrated for leukemia inhibitory factor, ciliary neurotrophic factor, and oncostatin M. Both of these effects are duplicated by addition o…

Superior cervical ganglionmedicine.medical_specialtyCell SurvivalRecombinant Fusion ProteinsSuperior Cervical GanglionCiliary neurotrophic factorPC12 CellsRats Sprague-DawleyMiceParacrine signallingContactinsInternal medicinemedicineAnimalsNerve Growth FactorsRNA MessengerInterleukin 6Autocrine signallingNeural Cell Adhesion MoleculesCells CulturedNeuronsMultidisciplinarybiologyInterleukin-6Neuropeptides3T3 CellsBiological SciencesReceptors Interleukin-6RatsCell biologyAutocrine CommunicationNerve growth factorEndocrinologyAnimals Newbornbiology.proteinNeural cell adhesion moleculeLeukemia inhibitory factorCaltech Library ServicesProceedings of the National Academy of Sciences
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The designer cytokine hyper-interleukin-6 is a potent activator of STAT3-dependent gene transcription in vivo and in vitro.

1999

Interleukin-6 (IL-6) triggers pivotal pathways in vivo. The designer protein hyper-IL-6 (H-IL-6) fuses the soluble IL-6 receptor (sIL-6R) through an intermediate linker with IL-6. The intracellular pathways that are triggered by H-IL-6 are not defined yet. Therefore, we studied the molecular mechanisms leading to H-IL-6-dependent gene activation. H-IL-6 stimulates haptoglobin mRNA expression in HepG2 cells, which is transcriptionally mediated as assessed by run-off experiments. The increase in haptoglobin gene transcription correlates with higher nuclear translocation of tyrosine-phosphorylated STAT3 and its DNA binding. As H-IL-6 stimulates STAT3-dependent gene transcription, we compared t…

Therapeutic gene modulationSTAT3 Transcription FactorTranscriptional ActivationTranscription GeneticRecombinant Fusion ProteinsResponse elementE-boxBiologyTransfectionBiochemistryCell LineMiceSp3 transcription factorAntigens CDCytokine Receptor gp130E2F1AnimalsHumansRNA MessengerPhosphorylationMolecular BiologyCell NucleusATF3Sp1 transcription factorMice Inbred C3HMembrane GlycoproteinsHaptoglobinsInterleukin-6Liver receptor homolog-1Biological TransportCell BiologyDNAReceptors InterleukinMolecular biologyReceptors Interleukin-6DNA-Binding ProteinsGene Expression RegulationTrans-ActivatorsTyrosineThe Journal of biological chemistry
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A novel and rapid prediction assay for the effectiveness of IL-6 receptor specific antisense oligonucleotides by proliferation inhibition of an inter…

2001

Interleukin-6 (IL-6) belongs to a family of cytokines that use receptors consisting of a common signal-transducing chain (gp130). Baf/3 cells transfected with the human IL-6 receptor (IL-6R) and gp130 (Baf/3-gp130/IL-6R) can only grow in medium containing IL-6. We attempted to interrupt the signal transducing pathway of IL-6 with the help of antisense oligonucleotides (ASOs) designed against the IL-6R. We used 18 different kinds of antisense oligonucleotides of overlapping sequences around the translational start codon of the human IL-6R. Sense ASOs were used as a control. The proliferation of cells was analysed by H-thymidine incorporation. Cell surface expression of the IL-6R was assessed…

Time FactorsCellBiologyCell LineSubstrate SpecificitySense (molecular biology)medicineHumansReceptorInterleukin 6Base SequenceInterleukin-6Cell BiologyGeneral MedicineTransfectionOligonucleotides AntisenseGlycoprotein 130Flow CytometryMolecular biologyReceptors Interleukin-6medicine.anatomical_structureCell cultureInterleukin-6 receptorbiology.proteinCell DivisionSignal TransductionCell biology international
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The aryl hydrocarbon receptor modulates acute and late mast cell responses.

2012

Abstract The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activity is modulated by xenobiotics as well as physiological ligands. These compounds may modulate inflammatory responses and contribute to the rising prevalence of allergic diseases observed in industrialized countries. Mast cells (MCs), located within tissues at the boundary of the external environment, represent a potential target of AhR ligands. In this study, we report that murine and human MCs constitutively express AhR, and its activation by the high-affinity ligand 6-formylindolo[3,2-b]carbazole (FICZ) determines a boost in degranulation. On the contrary, repeated exposure to FICZ inhibits…

Time FactorsInbred C57BLLigandsCell DegranulationPathogenesischemistry.chemical_compoundMiceAnaphylaxiReceptorsMast CellImmunology and AllergyMast CellsReceptorMice KnockoutbiologyInterleukin-17DegranulationMast cellUp-RegulationImmunology Mast Cell Aryl Receptormedicine.anatomical_structureAryl HydrocarbonBone Marrow Celldeficiency/metabolism/physiologyIgEmedicine.symptomimmunology/metabolism/pathologyHistamineHumanReceptorTime FactorKnockoutImmunologyDown-RegulationLigandInflammationBone Marrow CellsSettore MED/08 - Anatomia PatologicaCell LinebiosynthesiAnaphylaxis; immunology/metabolism/pathology Animals Bone Marrow Cells; immunology/metabolism/pathology Cell Degranulation; genetics/immunology Cell Line Down-Regulation; genetics/immunology Humans Interleukin-17; biosynthesis Interleukin-6; biosynthesis Ligands Mast Cells; immunology/metabolism/pathology Mice Mice; Inbred C57BL Mice; Knockout Receptors; Aryl Hydrocarbon; deficiency/metabolism/physiology Receptors; IgE; physiology Time Factors Up-Regulation; genetics/immunologymedicineAnimalsHumansTranscription factorAnaphylaxisAnimalInterleukin-6Receptors IgEAryl hydrocarbon receptorgenetics/immunologyMice Inbred C57BLMAST CELL; ARYL HYDROCARBON RECEPTORchemistryReceptors Aryl HydrocarbonImmunologyphysiologybiology.proteinbiosynthesisJournal of immunology (Baltimore, Md. : 1950)
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Il-6 signaling in inflammatory bowel disease: pathophysiological role and clinical relevance.

2007

Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory bowel diseases (IBDs) occurring in the gut of genetically susceptible individuals independent of a specific pathogen. The interaction between antigen-presenting cells and the local bacterial flora contributes to an uncontrolled activation of mucosal CD4+ T lymphocytes with the consecutive release of proinflammatory cytokines such as tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, IL-23, IL-27, and also IL-17, which is attributed to a specific, differentiated CD4+ lineage called Th17 (TH-IL17, THi). Recent data suggest that IL-6 contributes to Th17 differentiation. However, to clarify the importance of Th17 cel…

biologyInterleukin-6Interleukin-17GastroenterologyInterleukinInflammationApoptosismedicine.diseaseInflammatory Bowel DiseasesInflammatory bowel diseaseReceptors Interleukin-6Proinflammatory cytokineInterleukin-6 receptorImmunologymedicinebiology.proteinImmunology and AllergyAnimalsHumansTumor necrosis factor alphaInterleukin 17medicine.symptomInterleukin 6Signal TransductionInflammatory bowel diseases
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Endurance training induces apoptosis in the tumor mass in the C26-bearing mouse model

2018

colon carcinoma; metastasis; cachexia; Hsp60: interleukin-6metastasiscolon carcinomacachexiaHsp60: interleukin-6
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