Search results for "interleukin 6"

showing 10 items of 152 documents

P051 Macrophages as a source of Notch Ligands in Crohn’s disease: implications in fibrosis

2021

Abstract Background Fibrosis constitute the main complications associated to Crohn’s disease (CD). Notch signalling has been implicated in lung, kidney, liver and cardiac fibrosis. Macrophages contribute to fibrosis through the release of different mediators and the pattern of secretion may vary according to their microenvironment. The aim of the present study is to analyze the role of Notch ligands derived from macrophages in the complications of CD. Methods We have analyzed: the mRNA expression of cytokines and Notch ligands in CD patients with fistulizing and stenting pattern, the mRNA and protein expression of macrophage markers and Notch ligands in macrophages treated with the main cyt…

Crohn's diseasebiologybusiness.industrymedicine.medical_treatmentGastroenterologyVimentinGeneral Medicinemedicine.diseaseInterleukin 10CytokineFibrosismedicinebiology.proteinCancer researchSignal transductionInterleukin 6businessInterleukin 4Journal of Crohn's and Colitis
researchProduct

IL-6 stimulates annexin 1 expression and translocation and suggests a new biological role as class II acute phase protein.

1998

Annexin 1 (Ax 1), a protein whose synthesis and secretion are induced during the inflammatory response, has been proposed as a mediator of the anti-inflammatory action of glucocorticoids. To gain insight into a broader role of Ax 1 during the inflammatory response, the authors have investigated how pro-inflammatory cytokines [interleukin 1 (IL-1), IL-6 and tumour necrosis factor alpha (TNF-alpha)] affect Ax 1 expression and regulation at transcriptional and translational levels. The authors show that induction of the Ax 1 protein and its translocation to the cell membrane are stimulated by interleukin 6. However neither IL-1 nor TNF-alpha display these effects. Analysis of 5'-deletion mutan…

ElectrophoresisImmunologyAdenocarcinomaBiochemistryDexamethasoneMediatorAnnexinTumor Cells CulturedImmunology and AllergyHumansSecretionRNA MessengerCloning MolecularInterleukin 6Promoter Regions GeneticMolecular BiologyAnnexin A1Reporter genebiologyInterleukin-6Acute-phase proteinInterleukinNuclear ProteinsHematologyMolecular biologyRecombinant ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticMifepristonebiology.proteinCCAAT-Enhancer-Binding ProteinsMutagenesis Site-DirectedTumor necrosis factor alphaAcute-Phase ProteinsTranscription FactorsCytokine
researchProduct

AN IL-6/IL-6 SOLUBLE RECEPTOR (IL-6R) HYBRID PROTEIN (H-IL-6) INDUCES EPO-INDEPENDENT ERYTHROID DIFFERENTIATION IN HUMAN CD34+CELLS

2000

H-IL-6 is a hybrid protein constructed to contain IL-6 and its soluble receptor linked by a flexible peptide chain. Here we show that H-IL-6 strongly enhances proliferation of human CD34(+)cells in serum-free liquid culture, and that the majority of the cells generated belong to the erythroid lineage, being positive for the marker Glycophorin A. Conversely, H-IL-6 does not increase the number of myeloid, CD13-positive cells. Comparable effects are observed on progenitors from cord blood and adult peripheral blood. Therefore, H-IL-6 triggers an erythroid-inducing signal in haematopoietic progenitor cells, independently from erythropoietin (EPO).

ErythrocytesTime FactorsMyeloidCellular differentiationInterleukin 6Antigens CD34BiochemistryCulture Media Serum-FreeSerum-Freehemic and lymphatic diseasesReceptorsLeukocytesImmunology and AllergyErythropoiesisGlycophorinsStem Cell FactorbiologyChemistryCord bloodCell DifferentiationHematologyFetal BloodFlow CytometryEndothelial stem cellHaematopoiesismedicine.anatomical_structureGlycophorinCD34+medicine.drugRecombinant Fusion ProteinsMononuclearImmunologyCD13 AntigensmedicineHumansGlycophorinAntigensProgenitor cellErythropoietinMolecular BiologyInterleukin 3Interleukin-6CD34+; Cord blood; Erythropoiesis; Interleukin 6; Stem cell factor; Antigens CD34; CD13 Antigens; Cell Differentiation; Culture Media Serum-Free; Erythrocytes; Erythropoietin; Fetal Blood; Flow Cytometry; Glycophorin; Hematopoietic Stem Cells; Humans; Interleukin-6; Leukocytes Mononuclear; Peptides; Receptors Interleukin-6; Recombinant Fusion Proteins; Stem Cell Factor; Time Factors; Immunology and Allergy; Immunology; Biochemistry; Hematology; Molecular BiologyHematopoietic Stem CellsReceptors Interleukin-6Molecular biologyCulture MediaErythropoietinLeukocytes Mononuclearbiology.proteinCD34PeptidesCytokine
researchProduct

Immunological insights into the pathogenesis of active CMV infection in non-immunosuppressed critically ill patients.

2011

Dissociation of cytomegalovirus (CMV) DNA loads between the lower respiratory tract and blood, with high levels in the former compartment and low or undetectable levels in the latter, commonly occurs during active CMV infection in critically ill patients despite the presence of high frequencies of CMV-specific IFN-γ-producing CD8+ and CD4+ T cells in blood. Data presented in this case report suggest that inter-compartmental differences in interleukin-10 (IL-10) levels may, in part, explain the pathobiology of this phenomenon. In the absence of ganciclovir treatment, a significant correlation was observed between IL-10 levels and CMV DNA loads in lower respiratory tract specimens (P = 0.016)…

GanciclovirMalemedicine.medical_treatmentCritical IllnessRespiratory SystemCytomegalovirusPathogenesisVirologymedicineHumansInterleukin 6AgedAged 80 and overLungbiologyvirus diseasesImmunosuppressionMiddle AgedViral LoadVirologyInterleukin-10Interleukin 10Infectious Diseasesmedicine.anatomical_structureBloodImmunologyCytomegalovirus Infectionsbiology.proteinFemaleBronchoalveolar Lavage FluidCD8Respiratory tractmedicine.drugJournal of medical virology
researchProduct

IL-6 Signaling Promotes Tumor Growth in Colorectal Cancer

2004

Recent investigations support an important role for TGF-beta in the development of colorectal cancer. However, the molecular consequences of TGF-beta signaling in the colon remains incompletely understood. In a recent study in Immunity, we analyzed the role of TGF-beta in a murine model of colon cancer. Using transgenic mice overexpressing TGF-beta or a dominant negative TGF-beta receptor II under control of the CD2 minigene, we show that TGF-beta signaling in tumor infiltrating T lymphocytes regulates the growth of dysplastic colon epithelial cells, as determined by histology and a novel system for high resolution chromoendoscopy in vivo. At the molecular level, TGF-beta signaling in T cel…

Genetically modified mouseCell growthColorectal cancerCell BiologyBiologyEndoglinmedicine.diseaseTumor progressionIn vivoImmunologyCancer researchbiology.proteinmedicineADAM17 ProteinInterleukin 6Molecular BiologyDevelopmental BiologyCell Cycle
researchProduct

Astrocytic alterations in interleukin-6/Soluble interleukin-6 receptor alpha double-transgenic mice.

2000

Interleukin-6 (IL-6), a major cytokine with diverse effects on cells mainly of the immune and hematopoietic systems, has been linked to several neurological disorders such as acquired immune deficiency syndrome dementia, multiple sclerosis, and Alzheimer's disease. Central nervous system (CNS)-specific expression of IL-6 caused neurodegeneration, massive gliosis, and vascular proliferation in transgenic mice. However, the effects of systemically circulating IL-6 and its receptor IL-6Ralpha on the CNS are unknown. IL-6Ralpha is the specific component of the IL-6 receptor system and hence an important co-factor of IL-6. IL-6Ralpha is bioactive in a membrane-bound and in a soluble (s) form. We…

Genetically modified mouseCentral Nervous SystemPathologymedicine.medical_specialtyTransgeneCentral nervous systemGene ExpressionMice TransgenicBiologyPathology and Forensic MedicineMicemedicineAnimalsHumansTransgenesReceptorInterleukin 6Interleukin-6NeurodegenerationBrainmedicine.diseaseReceptors Interleukin-6Astrogliosismedicine.anatomical_structurePhenotypeGliosisSolubilityAstrocytesbiology.proteinmedicine.symptomRegular ArticlesThe American journal of pathology
researchProduct

TGF-β Suppresses Tumor Progression in Colon Cancer by Inhibition of IL-6 trans-Signaling

2004

Alterations of TGF-beta signaling have been described in colorectal cancer, although the molecular consequences are largely unknown. By using transgenic mice overexpressing TGF-beta or a dominant-negative TGF-betaRII, we demonstrate that TGF-beta signaling in tumor infiltrating T lymphocytes controls the growth of dysplastic epithelial cells in experimental colorectal cancer, as determined by histology and a novel system for high-resolution chromoendoscopy. At the molecular level, TGF-beta signaling in T cells regulated STAT-3 activation in tumor cells via IL-6. IL-6 signaling required tumor cell-derived soluble IL-6R rather than membrane bound IL-6R and suppression of such TGF-beta-depende…

Genetically modified mouseSTAT3 Transcription FactorColorectal cancerRecombinant Fusion ProteinsT-LymphocytesImmunologyBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicProtein Serine-Threonine KinasesMiceIn vivoTransforming Growth Factor betamedicineImmunology and AllergyAnimalsHumansEndoscopy Digestive SystemIntestinal MucosaInterleukin 6Autocrine signallingMice KnockoutbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionReceptor Transforming Growth Factor-beta Type IIHistologymedicine.diseaseImmunohistochemistryReceptors Interleukin-6DNA-Binding ProteinsDisease Models AnimalInfectious DiseasesTumor progressionImmunologyColonic NeoplasmsCancer researchbiology.proteinDisease ProgressionTrans-ActivatorsReceptors Transforming Growth Factor betaTransforming growth factorSignal TransductionImmunity
researchProduct

The designer cytokine hyper-IL-6 mediates growth inhibition and GM-CSF-dependent rejection of B16 melanoma cells.

2000

The low immunogenic B16 melanoma cell line was transfected with a mammalian expression vector containing the complementary DNA for a sIL-6R/IL-6 fusion protein, termed Hyper-IL-6 (H-IL-6), which was shown to have biological activities at 100-1000-fold lower concentrations than IL-6 in combination with sIL-6R. The secreted p84 glycoprotein was detected in the supernatant of transfected cells and was fully active on BAF3/gp130 cells, which respond to IL-6/sIL-6R but not to IL-6 alone. Administration of recombinant H-IL-6 to C57BL/6 mice resulted in a prolonged acute phase protein gene expression indicating long systemic persistence of the fusion protein. Transfected B16 cells (B16/H-IL6 cells…

Graft RejectionCancer ResearchTumor suppressor geneRatónmedicine.medical_treatmentRecombinant Fusion ProteinsMelanoma ExperimentalMice TransgenicTransfectionchemistry.chemical_compoundMiceGene expressionGeneticsmedicineAnimalsDrug InteractionsInterleukin 6neoplasmsMolecular BiologybiologyInterleukin-6MelanomaGranulocyte-Macrophage Colony-Stimulating FactorReceptors Interleukinmedicine.diseaseReceptors Interleukin-6Growth Inhibitorsrespiratory tract diseasesCytokinechemistryCell cultureReceptors Granulocyte-Macrophage Colony-Stimulating FactorImmunologybiology.proteinCancer researchGrowth inhibitionImmunosuppressive AgentsOncogene
researchProduct

Role of colony‐stimulating factors in the biology of acute myelogenous leukemia

1989

A high proportion of acute myeloid leukemias (AML) recently investigated for their capacity to synthesize biologically active bioregulatory molecules was found to accumulate messenger (m) RNA and to produce membrane-bound or -secreted forms of stimulating factors for granulocyte, macrophage and mixed granulocyte-macrophage colony growth. Blast cells have also been found to secrete interleukin 1, tumor necrosis factor-alpha, interleukin 6, and to express receptors for various growth factors as well. However, growth factors like interleukin 2 and interleukin 3 have not been identified as AML products, and several other factors including interleukin 4, interleukin 5, etc. need further evaluati…

Growth factormedicine.medical_treatmentInterleukinCell BiologyBiologyLeukemia Myeloid AcuteInterleukin 20Colony-Stimulating FactorsImmunologyCancer researchmedicineInterleukin 12biology.proteinHumansInterleukin 6Interleukin 5Interleukin 4Interleukin 3The International Journal of Cell Cloning
researchProduct

Possible role of human interleukin-6 and soluble interleukin-6 receptor in hepatitis B virus infection

2001

Human interleukin-6 has been shown to promote hepatitis B virus (HBV) infection. However, it is not clear whether this influence is the result of a direct interaction between interleukin-6 (IL-6) and the HBV envelope proteins or of a rather indirect mechanism. A direct interaction of IL-6 and the preS region of the large envelope protein (L-protein) of HBV has been reported. In this study we assessed the binding of IL-6 and of the IL-6 receptor subunits to the preS region of the L-protein of HBV. Binding of IL-6 and IL-6 receptor subunits sIL-6R and gp130 to preS was assessed by immunoprecipitation with recombinant preS proteins. In patient sera IL-6 and sIL-6R concentrations were analysed …

Hepatitis B virusmedicine.disease_causeHepatitis B virus PRE betalaw.inventionHepatitis B ChroniclawVirologyEscherichia colimedicineAnimalsHumansProtein PrecursorsInterleukin 6ReceptorCells CulturedHepatitis B virusHepatitis B Surface AntigensHepatologybiologyInterleukin-6Chemistryvirus diseasesViral LoadHepatitis BGlycoprotein 130medicine.diseasePrecipitin TestsReceptors Interleukin-6VirologyMolecular biologyRecombinant ProteinsInfectious DiseasesSolubilityCOS CellsRecombinant DNAbiology.proteinViral loadCell DivisionPlasmidsJournal of Viral Hepatitis
researchProduct