Search results for "Tumor necrosis factor-a."

showing 10 items of 505 documents

A Propensity Score-matched Comparison of Infliximab and Adalimumab in Tumour Necrosis Factor-α Inhibitor-naïve and Non-naïve Patients with Crohn's Di…

2019

Background and aims There is an unmet need to better understand the effectiveness of different biologics in inflammatory bowel diseases. We aimed at performing a multicentre, real-life comparison of the effectiveness of infliximab [IFX] and adalimumab [ADA] in Crohn's disease [CD]. Methods Data of consecutive patients with CD treated with IFX and ADA from January 2013 to May 2017 were extracted from the cohort of the Sicilian Network for Inflammatory Bowel Disease. We used propensity score-matching accounting for the main baseline characteristics in TNF-α inhibitor-naive and non-naive patients. Results A total of 632 patients [735 total treatments] were included. Among naive patients, a cli…

0301 basic medicineAdultMalemedicine.medical_specialtyInflammatory bowel diseaseGastroenterology03 medical and health sciencesYoung Adult0302 clinical medicineCrohn DiseaseGastrointestinal AgentsInternal medicinemedicineAdalimumabHumansYoung adultSicilypropensity scoreCrohn's diseasebusiness.industryTumor Necrosis Factor-alphaGastroenterologyAdalimumabGeneral MedicineOdds ratiomedicine.diseaseAdalimumab; infliximab; propensity score; Adalimumab; Adult; Crohn Disease; Female; Gastrointestinal Agents; Humans; Infliximab; Male; Propensity Score; Sicily; Treatment Outcome; Tumor Necrosis Factor-alpha; Young AdultInfliximab030104 developmental biologyTreatment OutcomeCohortPropensity score matching030211 gastroenterology & hepatologyFemalebusinessinfliximabmedicine.drug
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Hepatoprotective effects of extracts, fractions and compounds from the stem bark of Pentaclethra macrophylla Benth: Evidence from in vitro and in viv…

2021

Abstract Aim To identify the bioactive hepatoprotective components of the ethanol extract of Pentaclethra macrophylla stem bark using in vitro and in vivo approaches. Methods The bioguided-fractionation of the ethanol extract was based on the substances’ capacity to prevent in vitro, the lipid peroxidation of hepatocytes’ membranes induced by hydrogen peroxide. For the in vivo hepatoprotective test, mice were treated orally with the ethyl acetate (EtOAc) fraction of the ethanol extract at doses of 50 and 75 mg/kg/day for one week and subjected to d -galactosamine/lipopolysaccharide (GaIN/LPS)-induced hepatotoxicity. Blood samples were collected for alanine aminotransferase (ALAT), aspartate…

0301 basic medicineAntioxidantPentaclethra macrophyllaIsolated compoundsmedicine.medical_treatmentInterleukin-1betaLipid peroxidationStructure-activity relationshipsRM1-950AntioxidantsLipid peroxidationSuperoxide dismutase03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineIn vivomedicineAnimalsAspartate AminotransferasesRats WistarPharmacologybiologyTraditional medicinePlant StemsChemistryPlant ExtractsTumor Necrosis Factor-alphaBergeninAlanine TransaminaseFabaceaeGeneral MedicineGlutathioneDisease Models Animal030104 developmental biologyHepatoprotectionLiverCatalase030220 oncology & carcinogenesisbiology.proteinHepatocytesPlant BarkTherapeutics. PharmacologyChemical and Drug Induced Liver InjuryGaIN/LPSHepatoprotectionBiomedicine & Pharmacotherapy
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Secretion of autoimmune antibodies in the human subcutaneous adipose tissue

2018

The adipose tissue (AT) contributes to systemic and B cell intrinsic inflammation, reduced B cell responses and secretion of autoimmune antibodies. In this study we show that adipocytes in the human obese subcutaneous AT (SAT) secrete several pro-inflammatory cytokines and chemokines, which contribute to the establishment and maintenance of local and systemic inflammation, and consequent suboptimal immune responses in obese individuals, as we have previously shown. We also show that pro-inflammatory chemokines recruit immune cells expressing the corresponding receptors to the SAT, where they also contribute to local and systemic inflammation, secreting additional pro-inflammatory mediators.…

0301 basic medicineB CellsPhysiologylcsh:MedicineAutoimmunityPathology and Laboratory MedicineSystemic inflammationWhite Blood CellsAnimal CellsImmune PhysiologyPlasma cell differentiationAdipocytesMedicine and Health Scienceslcsh:ScienceImmune ResponseConnective Tissue CellsInnate Immune SystemMultidisciplinaryT CellsBody Fluids3. Good healthBloodmedicine.anatomical_structurePhysiological ParametersConnective TissueCytokinesChemokinesCellular TypesAnatomymedicine.symptomResearch ArticleLipolysisImmune CellsImmunologySubcutaneous FatInflammationBiology03 medical and health sciencesSigns and SymptomsImmune systemAntigenDiagnostic MedicinemedicineHumansObesityAntibody-Producing CellsB cellAutoantibodiesInflammationBlood CellsTumor Necrosis Factor-alphalcsh:RBody WeightAutoantibodyBiology and Life SciencesGerminal centerCell BiologyMolecular DevelopmentOxidative StressBiological Tissue030104 developmental biologyImmune SystemImmunologylcsh:QTranscription FactorsDevelopmental BiologyPLOS ONE
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Inhibition of colon cancer growth by docosahexaenoic acid involves autocrine production of TNFα

2016

IF 7.932; International audience; The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) has anti-inflammatory and anti-cancer properties. Among pro-inflammatory mediators, tumor necrosis factor a (TNF alpha) plays a paradoxical role in cancer biology with induction of cancer cell death or survival depending on the cellular context. The objective of the study was to evaluate the role of TNFa in DHA-mediated tumor growth inhibition and colon cancer cell death. The treatment of human colorectal cancer cells, HCT-116 and HCT-8 cells, with DHA triggered apoptosis in autocrine TNF alpha-dependent manner. We demonstrated that DHA-induced increased content of TNF alpha mRNA occurred thr…

0301 basic medicineCancer ResearchTumoricidal ActionApoptosis[ SDV.CAN ] Life Sciences [q-bio]/CancerMice[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsForkhead Box Protein O3Cell cycle3. Good healthCell biologyGene Expression Regulation NeoplasticAutocrine CommunicationColonic NeoplasmsTumor-Necrosis-FactorTumor necrosis factor alphaProgrammed cell deathDocosahexaenoic AcidsHuman Colorectal-CancerGene-Expression[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesGrowth factor receptorLipid-MetabolismGeneticsmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCell-DeathPolyunsaturated Fatty-AcidsAutocrine signallingMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyActivated Protein-KinaseTumor Necrosis Factor-alpha[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyInduced ApoptosisCancerHCT116 Cellsmedicine.diseaseXenograft Model Antitumor AssaysMicroRNAs030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsApoptosisCancer cellCancer researchPrevents Breast-Cancer
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Mast cells crosstalk with B cells in the gut and sustain IgA response in the inflamed intestine.

2021

B lymphocytes are among the cell types whose effector functions are modulated by mast cells (MCs). The B/MC crosstalk emerged in several pathological settings, notably the colon of inflammatory bowel disease (IBD) patients is a privileged site in which MCs and IgA+ cells physically interact. Herein, by inducing conditional depletion of MCs in red MC and basophil (RMB) mice, we show that MCs control B cell distribution in the gut and IgA serum levels. Moreover, in dextran sulfate sodium (DSS)-treated RMB mice, the presence of MCs is fundamental for the enlargement of the IgA+ population in the bowel and the increase of systemic IgA production. Since both conventional B-2 and peritoneal-deriv…

0301 basic medicineCell typeColon[SDV]Life Sciences [q-bio]ImmunologyPopulationInflammationBasophilBiologySettore MED/08 - Anatomia Patologicabehavioral disciplines and activitiesInflammatory bowel diseasecell-to-cell interplay colitis IgAinnate-like B cells mast cells03 medical and health sciencesMice0302 clinical medicinemedicineImmunology and AllergyAnimalsMast CellsColitisIntestinal MucosaeducationB cellComputingMilieux_MISCELLANEOUSInflammationeducation.field_of_studyB-LymphocytesTumor Necrosis Factor-alphaDextran Sulfatemedicine.diseaseColitisInflammatory Bowel DiseaseshumanitiesInnate-like B cellsGastrointestinal MicrobiomeImmunoglobulin AMice Inbred C57BLCrosstalk (biology)030104 developmental biologymedicine.anatomical_structureCell-to-cell interplayCell-to-cell interplay; Colitis; IgA; Innate-like B cells; Mast cellsImmunologymedicine.symptomIgA030215 immunologyEuropean journal of immunologyReferences
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Evolution of Ciona intestinalis Tumor necrosis factor alpha ( Ci TNFα): Polymorphism, tissues expression, and 3D modeling

2017

Although the Tumor necrosis factor gene superfamily seems to be very conserved in vertebrates, phylogeny, tissue expression, genomic and gene organization, protein domains and polymorphism analyses showed that a strong change has happened mostly in invertebrates in which protochordates were a constraint during the immune-molecules history and evolution. RT PCR was used to investigate differential gene expression in different tissues. The expression shown was greater in the pharynx. Single-nucleotide polymorphism has been investigated in Ciona intestinalis Tumor necrosis factor alpha (CiTNFα) mRNA isolated from the pharynx of 30 ascidians collected from Licata, Sicily (Italy), by denaturing …

0301 basic medicineCiona intestinaliIn silicoImmunologyProtein domainTNFSettore BIO/05 - ZoologiaPolymorphism Single NucleotideCiona intestinalis; DGGE; Gene expression; Polymorphism; TNF03 medical and health sciencesNegative selection0302 clinical medicineGene expressionAnimalsComputer SimulationCiona intestinalisRNA MessengerCloning MolecularSelection GeneticDGGEPolymorphismGeneCells CulturedPhylogenyGeneticsGenomebiologyTumor Necrosis Factor-alphaGene Expression ProfilingNucleic acid sequencebiology.organism_classificationBiological EvolutionMolecular biologyCiona intestinalis030104 developmental biologyPharynxGene expressionSequence Alignment030217 neurology & neurosurgeryTemperature gradient gel electrophoresisDevelopmental BiologyDevelopmental & Comparative Immunology
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1-ethyl-3-(6-methylphenanthridine-8-il) urea modulates TLR3/9 activation and induces selective pro-inflammatory cytokine expression in vitro.

2017

We have previously demonstrated the nucleic acid binding capacity of phenanthridine derivatives (PHTs). Because nucleic acids are potent inducers of innate immune response through Toll-like receptors (TLRs), and because PTHs bear a structural resemblance to commonly used synthetic ligands for TLR7/8, we hypothesized that PHTs could modulate/activate immune response. We found that compound M199 induces secretion of IL-6, IL-8 and TNFα in human PBMCs and inhibits TLR3/9 activation in different cellular systems (PBMCs, HEK293 and THP-1 cell lines).

0301 basic medicineClinical BiochemistryPharmaceutical ScienceDown-RegulationBiochemistryCell Line03 medical and health sciences0302 clinical medicineImmune systemDrug DiscoveryHumansImmunologic FactorsUreaSecretionReceptorMolecular BiologyInnate immune systemChemistryInterleukin-6Tumor Necrosis Factor-alphaOrganic ChemistryInterleukin-8Interferon-alphaTLR7Molecular biologyphenantridines ; TLR ; PBMCs ; cytokines ; immunomodulationIntercalating AgentsPhenanthridinesToll-Like Receptor 3030104 developmental biologyOligodeoxyribonucleotidesToll-Like Receptor 9TLR3Nucleic acidMolecular MedicineTumor necrosis factor alpha030215 immunologySignal TransductionBioorganicmedicinal chemistry letters
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Preventive effects of guanosine on intestinal inflammation in 2, 4-dinitrobenzene sulfonic acid (DNBS)-induced colitis in rats

2018

Background: Guanosine, a guanine-based purine, is an extracellular signaling molecule exerting anti-inflammatory and antioxidative effects in several in vivo and in vitro injury models. We aimed to investigate its protective effects on 2, 4-dinitrobenzene sulfonic acid (DNBS)-induced colitis in rat. Methods: Rats were divided into five groups and colitis was induced by intracolonic instillation of DNBS (15 mg/rat). Guanosine (4 or 8 mg/kg) was administered for 6 days i.p. starting the day of the colitis induction. Body weight loss, stool consistency, colon weight/length, histological analysis, myeloperoxidase activity (MPO) and pro-inflammatory cytokine levels were assessed. Immunoblotting …

0301 basic medicineDNBS ratColonmedicine.medical_treatmentInterleukin-1betaImmunologyAnti-Inflammatory AgentsGuanosineInflammationPharmacologySettore BIO/09 - FisiologiaInflammatory bowel diseaseAntioxidantsInflammatory bowel disease03 medical and health scienceschemistry.chemical_compound0302 clinical medicineIn vivomedicineAnimalsPharmacology (medical)Intestinal MucosaRats WistarColitisPurineInflammationPharmacologychemistry.chemical_classificationReactive oxygen speciesGuanosineInterleukin-6Tumor Necrosis Factor-alphaNF-kappa BColitismedicine.diseaseRats030104 developmental biologyCytokinechemistryCytokinesDinitrofluorobenzeneTumor necrosis factor alphamedicine.symptomReactive Oxygen Species030217 neurology & neurosurgeryInflammopharmacology
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A Pharmacological Update of Ellagic Acid.

2018

Este artículo se encuentra disponible en la página web de la revista en la siguiente URL: https://www.thieme-connect.com/products/ejournals/pdf/10.1055/a-0633-9492.pdf This is a pre-print of an article published in Ríos, JL., Giner, RM., Marín, M. and Recio, MC. (2018). A pharmacological update of ellagic acid. Planta Medica, vol. 84, n. 15, pp. 1068-1093. The final authenticated version is available online at: https://doi.org/10.1055/a-0633-9492 Este es el pre-print del siguiente artículo Ríos, JL., Giner, RM., Marín, M. and Recio, MC. (2018). A pharmacological update of ellagic acid. Planta Medica, vol. 84, n. 15, pp. 1068-1093 que se ha publicado de forma definitiva en https://doi.org/10…

0301 basic medicineEllagic acid - Pharmacokinetics.Antioxidantmedicine.medical_treatmentMetaboliteInterleukin-1betaAnti-Inflammatory AgentsPharmaceutical ScienceApoptosisPharmacologyProtective AgentsProteína quinasa.NeuroprotectionAntioxidantsAnalytical Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEllagic AcidGlycationDrug DiscoverymedicineHumansProtein kinases.Cell ProliferationPharmacologyMetabolic SyndromeAldose reductaseInterleukin-6Tumor Necrosis Factor-alphaMetabolismo - Trastornos.Organic ChemistryNF-kappa BLipid metabolismAtherosclerosisEllagic acid - Physiological effect.NeuroprotectionMetabolism disorder030104 developmental biologyComplementary and alternative medicinechemistryÁcido elágico - Efectos fisiológicos.Antioxidantes.Ácido elágico - Farmacocinética.030220 oncology & carcinogenesisMolecular MedicineMetabolism - Disorders.Antioxidants.Ellagic acidPlanta medica
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Role of the DNA repair glycosylase OGG1 in the activation of murine splenocytes

2017

OGG1 (8-oxoguanine-DNA glycosylase) is the major DNA repair glycosylase removing the premutagenic DNA base modification 8-oxo-7,8-dihydroguanine (8-oxoG) from the genome of mammalian cells. In addition, there is accumulating evidence that OGG1 and its substrate 8-oxoG might function in the regulation of certain genes, which could account for an attenuated immune response observed in Ogg1-/- mice in several settings. Indications for at least two different mechanisms have been obtained. Thus, OGG1 could either act as an ancillary transcription factor cooperating with the lysine-specific demethylase LSD1 or as an activator of small GTPases. Here, we analysed the activation by lipopolysaccaride…

0301 basic medicineGuanineDNA RepairDNA repairp38 mitogen-activated protein kinasesBiologyBiochemistryDNA GlycosylasesMice03 medical and health sciencesAnimalsMolecular BiologyTranscription factorTumor Necrosis Factor-alphaKinaseActivator (genetics)MacrophagesDNACell BiologyBase excision repairMolecular biology030104 developmental biologyGene Expression RegulationDNA glycosylaseTumor necrosis factor alphaSpleenDNA DamageTranscription FactorsDNA Repair
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