Search results for " cytokines"

showing 10 items of 104 documents

Interleukin 17 genes as mediators of inflammatory responses in Ciona intestinalis.

2015

Inflammation is a complex reaction of host defence mechanisms aiming at neutralization of an insult and restoring normal tissue structure and function. In human IL-17 is T-cell derived cytokine plays a key role in the clearance of extracellular bacteria promoting cell infiltration and production of several cytokines and chemokines. Here, we report on three Ciona intestinalis IL-17 homologues (CiIL17-1, CiIL17-2, CiIL17-3). The gene organization, phylogenetic tree and modeling supported the close relationship with the mammalian IL-17A and IL-17F suggesting that the C. intestinalis IL-17 genes share a common ancestor in the chordate lineages. Real time PCR analysis showed a prompt expression …

Inflammation Cytokines Ciona intestinalisSettore BIO/05 - Zoologia
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Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes

2015

Diabetic foot ulcerations have been extensively reported as vascular complications of diabetes mellitus associated with a high degree of morbidity and mortality. Diabetic foot syndrome (DFS), as defined by the World Health Organization, is an "ulceration of the foot (distally from the ankle and including the ankle) associated with neuropathy and different grades of ischemia and infection". Pathogenic events able to cause diabetic foot ulcers are multifactorial. Among the commonest causes of this pathogenic pathway it's possible to consider peripheral neuropathy, foot deformity, abnormal foot pressures, abnormal joint mobility, trauma, peripheral artery disease. Several studies reported how …

Inflammationmedicine.medical_specialtyPathologySettore MED/09 - Medicina InternaDiabetic foot syndrome; Inflammation; Cytokines; Cardiovascular risk; Markerbusiness.industryType 2 Diabetes MellitusType 2 diabetesDiseaseDiabetic foot syndromeMarkerCardiovascular riskmedicine.diseaseDiabetic footInsulin resistancePeripheral neuropathyInternal medicineDiabetes mellitusmedicineOrthopedics and Sports MedicineTopic HighlightbusinessCytokineFoot deformityWorld Journal of Orthopedics
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Multifunctional CD4(+) T cells correlate with active Mycobacterium tuberculosis infection.

2010

Th1 CD4(+) T cells and their derived cytokines are crucial for protection against Mycobacterium tuberculosis. Using multiparametic flow cytometry, we have evaluated the distribution of seven distinct functional states (IFN-gamma/IL-2/TNF-alpha triple expressors, IFN-gamma/IL-2, IFN-gamma/TNF-alpha or TNF-alpha/IL-2 double expressors or IFN-gamma, IL-2 or TNF-alpha single expressors) of CD4(+) T cells in individuals with latent M. tuberculosis infection (LTBI) and active tuberculosis (TB). We found that triple expressors, while detectable in 85-90%TB patients, were only present in 10-15% of LTBI subjects. On the contrary, LTBI subjects had significantly higher (12- to 15-fold) proportions of…

Interleukin 2AdultCD4-Positive T-LymphocytesMaleTuberculosisSettore MED/17 - Malattie InfettiveImmunologyCell SeparationBiologyLymphocyte ActivationFlow cytometryMycobacterium tuberculosis03 medical and health sciences0302 clinical medicineImmune systemBacterial ProteinsCD4(+) T cells Cytokines Mycobacterium tuberculosis infection Tuberculosis disease interferon-gamma immunological memory disease responses protection cytokine immunity bcg vaccination virusmedicineImmunology and AllergyDistribution (pharmacology)HumansCytokineTuberculosis Pulmonary030304 developmental biologyTuberculosis disease.Settore MED/04 - Patologia Generale0303 health sciencesAntigens Bacterialmedicine.diagnostic_testMycobacterium tuberculosis infectionMycobacterium tuberculosisMiddle Agedbiology.organism_classificationmedicine.diseaseFlow CytometryPhenotypeVirologyCD4+ T cellsBacterial Load3. Good healthImmunologyAcute DiseaseChronic DiseaseCytokinesTumor necrosis factor alphaAcyltransferases030215 immunologymedicine.drugEuropean journal of immunology
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Pivotal advance: alpha-galactosylceramide induces protection against lipopolysaccharide-induced shock.

2007

Abstract α−galactosylceramide, a natural killer T cell ligand, and its synthetic homolog, KRN7000, consistently influence IFN-γ and TNF-α release, both mediators of LPS-induced shock. To modify the course of endotoxin shock, we injected KRN7000 at different time points of experimental systemic Shwartzman reaction. Mice treated with KRN7000 survived when it was injected within 2 h before and after LPS challenge. Mice survival was associated with low levels of T helper 1 (Th1) cytokines, such as IFN-γ and TNF-α. By contrast, protection from endotoxin shock was associated with an increase of T helper 2 (Th2) cytokines, like IL-4 and IL-10. A role of Th2 cytokines in counteracting LPS-induced s…

LipopolysaccharidesMaleLipopolysaccharideImmunologyStimulationGalactosylceramidesBiologychemistry.chemical_compoundMiceStructure-Activity RelationshipTh2 CellsIn vivomedicineImmunology and AllergyAnimalsrodent cytokines endotoxinT-cell receptorCell BiologyTh1 CellsLigand (biochemistry)Natural killer T cellShock SepticKiller Cells NaturalMice Inbred C57BLDisease Models AnimalchemistryShock (circulatory)Immunologybiology.proteinDisease ProgressionCytokinesmedicine.symptomAntibodyShwartzman Phenomenon
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Quaking and miR-155 interactions in inflammation and leukemogenesis.

2015

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas …

LipopolysaccharidesTime Factorsmedicine.medical_treatmentmedicine.disease_causeTransgenicMiceInnatePhosphorylationChronicB-LymphocytesLeukemiaRNA-Binding ProteinsU937 CellsLymphocyticCell biologyCytokineOncologyPhosphorylationCytokinesCLL; Glioblastoma; Inflammation; MiR-155; QKI; Animals; Apoptosis Regulatory Proteins; B-Lymphocytes; Case-Control Studies; Cytokines; Humans; Immunity Innate; Inflammation; Leukemia Lymphocytic Chronic B-Cell; Lipopolysaccharides; Macrophages; Mice; Mice Transgenic; MicroRNAs; Mitogen-Activated Protein Kinases; Phosphorylation; RAW 264.7 Cells; RNA-Binding Proteins; Signal Transduction; Time Factors; Transfection; U937 Cells; OncologySignal transductionMitogen-Activated Protein KinasesSignal Transductionp38 mitogen-activated protein kinasesOncology and CarcinogenesisMice TransgenicTransfectionNOmiR-155miR-155Downregulation and upregulationmicroRNAmedicineAnimalsHumansInflammationQKIbusiness.industryMacrophagesB-CellImmunityglioblastomaLeukemia Lymphocytic Chronic B-CellImmunity InnateMicroRNAsRAW 264.7 CellsCase-Control StudiesImmunologyCarcinogenesisbusinessApoptosis Regulatory ProteinsCLLPriority Research Paper
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CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor-beta-dependent manner.

2007

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, redu…

MESH : CytokinesMESH: Flow CytometryMESH : Immunity NaturalMESH: T-LyLymphocyte ActivationT-Lymphocytes RegulatoryMiceInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsMESH : Receptors ImmunologicMESH : Cell ProliferationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH: NeoplasmsIL-2 receptorReceptors Immunologic0303 health sciencesMESH: Cytokineshemic and immune systemsFlow CytometryNatural killer T cell3. Good healthCell biologyKiller Cells Naturalmedicine.anatomical_structureNK Cell Lectin-Like Receptor Subfamily KInterleukin 12CytokinesReceptors Natural Killer Cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyFranceMESH : Killer Cells NaturalMESH : Cytotoxicity Tests ImmunologicMESH: Killer Cells NaturalMESH: Cell Line TumorMESH : Flow CytometryImmunologychemical and pharmacologic phenomenaMESH: Cytotoxicity Tests ImmunologicMESH : Mice Inbred C57BLBiologyArticleNatural killer cell03 medical and health sciencesMESH: Mice Inbred C57BLCell Line TumorMESH: Cell ProliferationMESH : MicemedicineAnimalsHumansAntigen-presenting cellMESH: Lymphocyte ActivationMESH : FranceMESH: MiceMESH: Receptors ImmunologicMESH : Lymphocyte ActivationCell Proliferation030304 developmental biologyMESH: Immunity NaturalLymphokine-activated killer cellMESH: HumansMESH : Cell Line TumorMESH : HumansCytotoxicity Tests ImmunologicNKG2DMESH : T-LyMESH : NeoplasmsImmunity InnateMice Inbred C57BLMESH: FranceMESH : Animals030215 immunology
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Mesenchymal stem cells derived from inflamed dental pulpal and gingival tissue: a potential application for bone formation

2017

Background Chronic periodontal disease is an infectious disease consisting of prolonged inflammation of the supporting tooth tissue and resulting in bone loss. Guided bone regeneration procedures have become common and safe treatments in dentistry, and in this context dental stem cells would represent the ideal solution as autologous cells. In this study, we verified the ability of dental pulp mesenchymal stem cells (DPSCs) and gingival mesenchymal stem cells (GMSCs) harvested from periodontally affected teeth to produce new mineralized bone tissue in vitro, and compared this to cells from healthy teeth. Methods To characterize DPSCs and GMSCs, we assessed colony-forming assay, immunophenot…

Male0301 basic medicinePathologyCellular differentiationGingivaMedicine (miscellaneous)Bone tissue0302 clinical medicineOsteogenesisMedicinelcsh:QD415-436Pulpal and gingival mesenchymal stem cellsCells CulturedStem cell transplantation for articular cartilage repairlcsh:R5-920Heat shock proteinCell DifferentiationADFsMiddle AgedGingivitismedicine.anatomical_structureBone formationMolecular MedicineFemaleStem celllcsh:Medicine (General)Adultmedicine.medical_specialtyAdolescentBiochemistry Genetics and Molecular Biology (miscellaneous)Proinflammatory cytokinelcsh:Biochemistry03 medical and health sciencesstomatognathic systemHumansPeriodontitisBone regenerationDental PulpAgedProinflammatory cytokinesInflammationbusiness.industryResearchMesenchymal stem cellMesenchymal Stem Cells030206 dentistryCell BiologyDental diseaseInflammation Dental disease Pulpal and gingival mesenchymal stem cells Bone formation Heat shock protein ADFs Proinflammatory cytokinesstomatognathic diseases030104 developmental biologyCancer researchPulp (tooth)businessStem Cell Research & Therapy
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Polymorphisms of Pro-Inflammatory IL-6 and IL-1β Cytokines in Ascending Aortic Aneurysms as Genetic Modifiers and Predictive and Prognostic Biomarkers

2021

Background: Previous studies have demonstrated that polymorphisms involved in immune genes can affect the risk, pathogenesis, and outcome of thoracic ascending aortic aneurysms (TAAA). Here, we explored the potential associations of five functional promoter polymorphisms in interleukin-6 (IL-6), IL-1B, IL-1A, IL-18, and Tumor necrosis factor (TNF)A genes with TAAA. Methods: 144 TAAA patients and 150 age/gender matched controls were typed using KASPar assays. Effects on telomere length and levels of TAAA related histopathological and serological markers were analyzed. Results: Significant associations with TAAA risk were obtained for IL-6 rs1800795G&gt

Male0301 basic medicinemedicine.medical_specialtyInterleukin-1betamedial cell apoptosisSingle-nucleotide polymorphism030204 cardiovascular system & hematologyrs16944MicrobiologyPolymorphism Single NucleotideBiochemistryGastroenterologyArticleProinflammatory cytokinePathogenesis03 medical and health sciences0302 clinical medicineAneurysmInternal medicineGenotypeelastic fragmentationmedicinetelomere lengthHumansInterleukin 6thoracic ascending aortic aneurysmsMolecular BiologyAgedAortic Aneurysm ThoracicbiologyInterleukin-6business.industryMMP9Prognosismedicine.diseasers1800795QR1-502Settore MED/23030104 developmental biologyproinflammatory cytokinescystic medial changesbiology.proteinCytokinesBiomarker (medicine)FemaleTumor necrosis factor alphaInflammation MediatorsbusinessBiomarkersBiomolecules
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Inflammatory activation and endothelial dysfunction markers in patients with permanent atrial fibrillation: A cross-sectional study

2020

In recent years a growing body of evidence supported the role of inflammation in the initiation, maintenance and outcome of atrial fibrillation (AF). Nevertheless, despite a large amount of information, whether AF or the underlying structural heart disease (SHD) is the cause of the inflammatory process is still under debate. We, therefore, sought to determine if the inflammatory process reflect an underlying disease or the arrhythmia 'per se'. We evaluated plasma levels of soluble Interleukin 2 Receptor Alpha (sIL-2Rα), TNF-α and IL-18 in 100 consecutive patients with permanent AF, (43 with a SHD and 57 without a SHD) compared to 121 age and sex-matched controls which had normal sinus rhyth…

MaleAgingmedicine.medical_specialtyHeart diseaseAlpha (ethology)InflammationDiseaseSystemic inflammationendothelial dysfunctionInternal medicineAtrial FibrillationmedicineHumansEndothelial dysfunctionReactive hyperemiaAgedAged 80 and overInflammationTumor Necrosis Factor-alphabusiness.industryInterleukin-18Interleukin-2 Receptor alpha SubunitAtrial fibrillationAtrial fibrillation Cytokines Endothelial dysfunction Inflammation Structural heart diseaseCell BiologyMiddle Agedmedicine.diseasestructural heart diseasecytokinesCross-Sectional StudiesLogistic ModelsROC CurveCase-Control StudiesCardiologyFemaleEndothelium Vascularmedicine.symptombusinessBiomarkersResearch Paper
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RORC1 Regulates Tumor-Promoting "Emergency" Granulo-Monocytopoiesis

2015

Cancer-driven granulo-monocytopoiesis stimulates expansion of tumor promoting myeloid populations, mostly myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs). We identified subsets of MDSCs and TAMs based on the expression of retinoic-acid-related orphan receptor (RORC1/RORγ) in human and mouse tumor bearers. RORC1 orchestrates myelopoiesis by suppressing negative (Socs3 and Bcl3) and promoting positive (C/EBPβ) regulators of granulopoiesis, as well as the key transcriptional mediators of myeloid progenitor commitment and differentiation to the monocytic/macrophage lineage (IRF8 and PU.1). RORC1 supported tumor-promoting innate immunity by protecting MDSCs from …

MaleCancer ResearchMyeloidNeutrophilsMacrophageCellular differentiationApoptosisMonocyteMonocyteshemic and lymphatic diseasesMyeloid CellsSOCS3Myeloid CellMyelopoiesisMice KnockoutMicroscopy ConfocalReverse Transcriptase Polymerase Chain ReactionMedicine (all)NeutrophilCell DifferentiationNuclear Receptor Subfamily 1 Group F Member 3Animals; Apoptosis; Cell Differentiation; Cell Line Tumor; Cytokines; Female; Gene Expression Regulation Neoplastic; Granulocytes; Humans; Immunohistochemistry; Macrophages; Male; Mice 129 Strain; Mice Inbred C57BL; Mice Knockout; Microscopy Confocal; Monocytes; Myeloid Cells; Myelopoiesis; Neoplasms Experimental; Neutrophils; Nuclear Receptor Subfamily 1 Group F Member 3; Reverse Transcriptase Polymerase Chain Reaction; Tumor Burden; Cancer Research; Cell Biology; Oncology; Medicine (all)ImmunohistochemistryTumor BurdenGene Expression Regulation NeoplasticHaematopoiesismedicine.anatomical_structureOncologyCytokinesFemaleMyelopoiesisHumanMice 129 StrainBiologySettore MED/08 - Anatomia PatologicaGranulopoiesisArticleMyelopoiesiCell Line TumormedicineAnimalsHumansCytokineInnate immune systemAnimalMacrophagesApoptosiGranulocyteNeoplasms ExperimentalCell BiologyMice Inbred C57BLImmunologyCancer researchIRF8Granulocytes
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