Search results for " CYTOKINE"

showing 10 items of 602 documents

Pentoxifylline Prevents Loss of PP2A Phosphatase Activity and Recruitment of Histone Acetyltransferases to Proinflammatory Genes in Acute Pancreatitis

2009

Mitogen-activated protein kinases (MAPKs) are considered major signal transducers early during the development of acute pancreatitis. Pentoxifylline is a phosphodiesterase inhibitor with marked anti-inflammatory properties through blockade of extracellular signal regulated kinase (ERK) phosphorylation and tumor necrosis factor alpha production. Our aim was to elucidate the mechanism of action of pentoxifylline as an anti-inflammatory agent in acute pancreatitis. Necrotizing pancreatitis induced by taurocholate in rats and taurocholate-treated AR42J acinar cells were studied. Phosphorylation of ERK and ERK kinase (MEK1/2), as well as PP2A, PP2B, and PP2C serine/threonine phosphatase activiti…

MaleMAPK/ERK pathwayChromatin ImmunoprecipitationPhosphodiesterase InhibitorsBlotting WesternPhosphataseAnti-Inflammatory AgentsPharmacologyBiologyCell LinePentoxifyllineProinflammatory cytokineCyclic AMPPhosphoprotein PhosphatasesmedicineAnimalsPentoxifyllineRats WistarExtracellular Signal-Regulated MAP KinasesHistone AcetyltransferasesInflammationPharmacologyReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaProtein phosphatase 2medicine.diseaseCyclic Nucleotide Phosphodiesterases Type 2RatsEnzyme ActivationPancreatitisBiochemistryAcute DiseaseRNAMolecular MedicinePhosphorylationPancreatitisMitogen-Activated Protein KinasesChromatin immunoprecipitationmedicine.drugJournal of Pharmacology and Experimental Therapeutics
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Human CD8+ T-cells Recognizing Peptides from Mycobacterium tuberculosis (Mtb) Presented by HLA-E Have an Unorthodox Th2-like, Multifunctional, Mtb In…

2015

Mycobacterial antigens are not exclusively presented to T-cells by classical HLA-class Ia and HLA-class II molecules, but also through alternative antigen presentation molecules such as CD1a/b/c, MR1 and HLA-E. We recently described mycobacterial peptides that are presented in HLA-E and recognized by CD8+ T-cells. Using T-cell cloning, phenotyping, microbiological, functional and RNA-expression analyses, we report here that these T-cells can exert cytolytic or suppressive functions, inhibit mycobacterial growth, yet express GATA3, produce Th2 cytokines (IL-4,-5,-10,-13) and activate B-cells via IL-4. In TB patients, Mtb specific cells were detectable by peptide-HLA-E tetramers, and IL-4 and…

MaleMacrophageQH301-705.5ImmunologyAntigen presentationBacterial ProteinMycobacterium tuberculosiHuman leukocyte antigenGATA3 Transcription FactorCD8-Positive T-LymphocytesMicrobiologyMicrobiologyMycobacterium tuberculosisImmune systemTh2 CellsGeneticHLA-EBacterial ProteinsVirologyGeneticsCytotoxic T cellHumansBiology (General)Th2 CellCytokineMolecular BiologyAntigen PresentationbiologyMacrophagesHistocompatibility Antigens Class ICD8-Positive T-LymphocyteMycobacterium tuberculosisRC581-607biology.organism_classificationBacterial Proteins; CD8-Positive T-Lymphocytes; Cytokines; Female; GATA3 Transcription Factor; Histocompatibility Antigens Class I; Humans; Macrophages; Male; Mycobacterium tuberculosis; Peptides; Th2 Cells; Antigen Presentation; Microbiology; Parasitology; Virology; Immunology; Genetics; Molecular BiologyPhenotypeVirology3. Good healthPeptideCytokinesParasitologyFemaleImmunologic diseases. AllergyPeptidesCD8HumanResearch ArticlePLoS Pathogens
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Autoimmune skin inflammation is dependent on plasmacytoid dendritic cell activation by nucleic acids via TLR7 and TLR9

2010

Lupus-prone mice develop a chronic inflammatory response to cutaneous injury that depends on the production of type I interferon, TLR7, and TLR9.

MaleMice 129 StrainImmunologyGene ExpressionInflammationchemical and pharmacologic phenomenaMice Inbred StrainsReceptor Interferon alpha-betaBiologySkin DiseasesArticleProinflammatory cytokinePathogenesisTLR9MiceAutoimmune skin inflammationimmune system diseasesNucleic AcidsmedicineImmunology and AllergyAnimalsLupus Erythematosus SystemicReceptorskin and connective tissue diseasesTLR7SkinAutoimmune skin inflammation; TLR7; TLR9; plasmacytoid dendritic cells.Mice KnockoutPlasmacytoid dendritic cell activationLupus erythematosusReverse Transcriptase Polymerase Chain ReactionTLR9virus diseaseshemic and immune systemsTLR7DNADendritic Cellsmedicine.diseaseFlow CytometryMice Inbred C57BLplasmacytoid dendritic cells.Toll-Like Receptor 7Toll-Like Receptor 9ImmunologyMyeloid Differentiation Factor 88CytokinesFemalemedicine.symptomThe Journal of Experimental Medicine
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Prevention of the post-chemotherapy relapse of tuberculous infection by combined immunotherapy

2008

Summary We report that a recently developed combined immunotherapy (CIT) has the capacity to prevent a spontaneous relapse of replicating Mycobacterium tuberculosis bacilli in the lungs of BALB/c, C57Bl/6 or C3H/HeJ strains of mice, following 4 weeks of non-sterilising treatment with isoniazid and rifampicin. The CIT regimen, represented by recombinant IFNγ, anti-α crystalline monoclonal IgA antibody and IL-4 neutralizing polyclonal antibody, reduced the 8-week relapse of viable bacterial counts in the lungs most significantly, when CIT was inoculated during the 5th week post infection, i.e. during the 3rd week of chemotherapy. Although CIT enhanced lung granuloma area, nitric oxide, cytoki…

MaleMicrobiology (medical)TuberculosisTuberculosiAntibodiemedicine.medical_treatmentImmunologyAntitubercular AgentsColony Count MicrobialMicrobiologyAntibodiesMycobacterium tuberculosisInterferon-gammaMiceAdjuvants ImmunologicRecurrencemedicineAnimalsalpha-CrystallinsRelapseTuberculosis PulmonaryCytokineMice Inbred BALB CMice Inbred C3HChemotherapyLungbiologybusiness.industryTuberculosis; Cytokines; Antibodies; Immunotherapy; RelapseIsoniazidMycobacterium tuberculosisImmunotherapybiology.organism_classificationmedicine.diseaseCombined Modality TherapyRecombinant ProteinsImmunoglobulin AMice Inbred C57BLRegimenInfectious Diseasesmedicine.anatomical_structureModels AnimalImmunologyInterleukin-4ImmunotherapybusinessRifampicinmedicine.drugTuberculosis
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MyD88 is dispensable for resistance toParacoccidioides brasiliensisin a murine model of blood-borne disseminated infection

2008

We have studied the role of MyD88, an adaptor protein of Toll-like receptors (TLRs), in murine defenses against Paracoccidioides brasiliensis in a model of blood-borne disseminated infection. Wild-type (WT) and MyD88-deficient mice infected intravenously with P. brasiliensis yeast cells showed an equivalent fungal burden, as well as similar levels of proinflammatory IL-1beta, IL-6, IL-12p70, tumor necrosis factor (TNF)-alpha and MIP-2, T-helper type 1 (Th1) (IFN-gamma) and Th2 cytokines (IL-4) in tissue homogenates. In vitro production of TNF-alpha, IFN-gamma and IL-12p70, by antigen-stimulated splenocytes from infected animals, was also similar in both types of mice; this production of Th1…

MaleMicrobiology (medical)medicine.medical_treatmentImmunologyNerve Tissue ProteinsMicrobiologyParacoccidioidesMicrobiologyProinflammatory cytokineMicePeritoneal cavitymedicineAnimalsHumansImmunology and AllergyLectins C-TypeMice KnockoutParacoccidioides brasiliensisbiologyMembrane ProteinsParacoccidioidesGeneral MedicineTh1 Cellsbiology.organism_classificationToll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4Disease Models AnimalTLR2Infectious Diseasesmedicine.anatomical_structureCytokineMyeloid Differentiation Factor 88Macrophages PeritonealTLR4CytokinesTumor necrosis factor alphaParacoccidioidomycosisFungemiaFEMS Immunology & Medical Microbiology
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Interferon-γ Induces Chronic Active Myocarditis and Cardiomyopathy in Transgenic Mice

2007

Chronic heart failure is associated with an activation of the immune system characterized among other factors by the cardiac synthesis and serum expression of proinflammatory cytokines. There is unequivocal clinical and experimental evidence that the cytokine tumor necrosis factor-alpha is involved in the development of chronic heart failure, but a putative cardiotoxic potential of the proinflammatory cytokine interferon (IFN)-gamma remains primarily unknown. To investigate this issue we analyzed the cardiac phenotype of SAP-IFN-gamma transgenic mice, which constitutively express IFN-gamma in their livers and hence exhibit high circulating serum levels of this cytokine. SAP-IFN-gamma mice s…

MaleMyocarditismedicine.medical_treatmentT-LymphocytesCardiomyopathyGene ExpressionMice Inbred StrainsMice Transgenic030204 cardiovascular system & hematologyBiologyPathology and Forensic MedicineProinflammatory cytokine03 medical and health sciencesInterferon-gammaMice0302 clinical medicinemedicineAnimalsHumansInterferon gammaIntestinal MucosaPromoter Regions Genetic030304 developmental biology0303 health sciencesCardiotoxicityReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaMacrophagesHeartDendritic Cellsmedicine.diseaseInterleukin-123. Good healthRatsIntestinesMice Inbred C57BLMyocarditisSerum Amyloid P-ComponentCytokineEchocardiographyImmunologyChronic DiseaseInterleukin 12Tumor necrosis factor alphaFemaleCardiomyopathiesmedicine.drugRegular Articles
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CCR5 Proinflammatory Allele in Prostate Cancer Risk

2009

Prostate cancer (PCa) is the most common malignant neoplasm in older men in Western countries. The number of affected older men is increasing. Therefore, strategies for prevention of prostate cancer are crucial. To this purpose it is essential to know the mechanisms involved in development and progression of this malignancy. Recently, an increasing body of genetic and epidemiological studies proposed new hypotheses for prostate carcinogenesis. It has been suggested that genetic factors as well as exposure to environmental factors such as infectious agents, dietary carcinogens, and hormonal imbalances participate in PCa development. Besides, chronic inflammation plays a key role in PCa. Taki…

MaleOncologyProstate Cancer Inflammation CCR5delta32 deletionmedicine.medical_specialtyReceptors CCR5Pilot ProjectsInflammationBiologyMalignancyGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineProstate cancerHistory and Philosophy of ScienceProstateInternal medicineMolecular geneticsEpidemiologymedicineHumansAlleleAllelesAgedSettore MED/04 - Patologia GeneraleAged 80 and overGeneral NeuroscienceProstatic Neoplasmsmedicine.diseasemedicine.anatomical_structureImmunologyInflammation Mediatorsmedicine.symptomAnnals of the New York Academy of Sciences
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Comparative impact of multiple biomarkers and N-terminal pro-brain natriuretic peptide in the context of conventional risk factors for the prediction…

2006

Background— Individual markers of inflammation may add incremental predictive value in the context of conventionally available risk factors. We evaluated the ability of 9 inflammatory biomarkers, microalbuminuria, and N-terminal pro-brain natriuretic peptide (Nt-proBNP) to improve cardiovascular risk prediction beyond that obtained from traditional risk factors in a secondary-prevention population. Methods and Results— We measured biomarkers representing the acute-phase reaction (C-reactive protein, fibrinogen, and interleukin-6), proinflammatory pathways (soluble tumor necrosis factor receptor-1 and -2, soluble interleukin-1 receptor antagonist, and interleukin-18), endothelial activation…

MaleOncologymedicine.medical_specialtyHeart Diseasesmedicine.drug_classPopulationMyocardial InfarctionAngiotensin-Converting Enzyme InhibitorsContext (language use)Coronary Artery DiseaseProinflammatory cytokineEndothelial activationRamiprilPredictive Value of TestsRisk FactorsPhysiology (medical)Internal medicineNatriuretic Peptide BrainNatriuretic peptideHumansVitamin EMedicineRisk factoreducationAgededucation.field_of_studyInterleukin-6business.industryFibrinogenMiddle Agedmedicine.diseaseBrain natriuretic peptideC-Reactive ProteinEndocrinologyFemaleMicroalbuminuriaCardiology and Cardiovascular MedicinebusinessBiomarkers
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Disseminated tuberculosis in a patient treated with a JAK2 selective inhibitor: a case report

2012

Abstract Background Primary myelofibrosis is a myeloproliferative disorder characterized by bone marrow fibrosis, abnormal cytokine expression, splenomegaly and anemia. The activation of JAK2 and the increased levels of circulating proinflammatory cytokines seem to play an important role in the pathogenesis of myelofibrosis. Novel therapeutic agents targeting JAKs have been developed for the treatment of myeloproliferative disorders. Ruxolitinib (INCB018424) is the most recent among them. Case presentation To our knowledge, there is no evidence from clinical trials of an increased risk of tuberculosis during treatment with JAK inhibitors. Here we describe the first case of tuberculosis in a…

MaleOncologymedicine.medical_specialtyRuxolitinibTuberculosisSettore MED/17 - Malattie InfettiveAnemiaAntitubercular AgentsMyelofibrosislcsh:MedicineCase ReportGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineMyeloproliferative DisordersInternal medicineNitrilesmedicineHumansTuberculosisMyelofibrosislcsh:Science (General)lcsh:QH301-705.5Medicine(all)Janus kinase 2biologyLatent tuberculosisBiochemistry Genetics and Molecular Biology(all)business.industryTuberculosis Myelofibrosis Ruxolitiniblcsh:RGeneral MedicineJanus Kinase 2medicine.diseasePyrimidinesRuxolitiniblcsh:Biology (General)Primary MyelofibrosisImmunologybiology.proteinPyrazolesbusinessmedicine.druglcsh:Q1-390BMC Research Notes
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Expression of Interleukin-32 in the Inflamed Arteries of Patients With Giant Cell Arteritis

2011

Objective Giant cell (temporal) arteritis (GCA) is a vasculitis that mainly affects the large and medium arteries, especially the branches of the proximal aorta. Interleukin-32 (IL-32) is a recently described Th1 proinflammatory cytokine, and is mainly induced by interferon-γ (IFNγ), IL-1β, and tumor necrosis factor α (TNFα). This study was undertaken to investigate the expression and tissue distribution of IL-32 in artery biopsy specimens from patients with GCA. Methods Quantitative gene expression analysis of IL-32, IL-1β, TNFα, IFNγ, IL-6, and IL-27 was performed in artery biopsy specimens obtained from 18 patients with GCA and 15 controls. Immunohistochemistry analysis was performed to …

MalePathologyInterleukin-1betaMessenger80 and overImmunology and AllergyPharmacology (medical)Giant Cell ArteritiAged 80 and overeducation.field_of_studyReverse Transcriptase Polymerase Chain ReactionInterleukin-17StatisticsArteriesMiddle AgedFlow CytometryImmunohistochemistryTh1 responseFemaleInterleukin 17VasculitisInterleukin-32; Giant Cell Arteritis; Th1 responsemedicine.medical_specialtyGiant Cell ArteritisImmunologyPopulationBiologyStatistics NonparametricProinflammatory cytokineInterferon-gammaRheumatologymedicine.arterymedicineHumansNonparametricRNA MessengerArteritiseducationAgedAortaAged; Aged 80 and over; Arteries; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; Interferon-gamma; Interleukin-17; Interleukin-1beta; Interleukin-6; Interleukins; Male; Middle Aged; RNA Messenger; Reverse Transcriptase Polymerase Chain Reaction; Statistics Nonparametric; Th1 Cells; Tumor Necrosis Factor-alphaInterleukin-6Tumor Necrosis Factor-alphaInterleukinsTh1 Cellsmedicine.diseaseInterleukin-32Giant cell arteritisGiant cellImmunologyRNA
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