Search results for "Tumor necrosis factor"

showing 10 items of 849 documents

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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Clinical efficacy of α4 integrin block with natalizumab in ankylosing spondylitis

2016

We describe the impact of α4-β1/7 blockade with natalizumab, a recombinant humanised immunoglobulin (Ig) G4κ monoclonal antibody (mAb) targeted to the α4 subunit of the α4β1 and α4β7 integrins, on the gut and spine inflammation in a patient with ankylosing spondylitis (AS) who developed multiple sclerosis after treatment with tumour necrosis factor (TNF)-blocking agents. A 45-year-old man with human leucocyte antigen (HLA)-B27-positive AS was admitted in January 2007. He had been diagnosed with AS 4 years earlier based on the presence of inflammatory back pain, peripheral arthritis, radiographic bilateral grade 2 sacroiliitis, HLA-B27 positivity. At that time, he had evidence of chronic int…

0301 basic medicineGenetics and Molecular Biology (all)medicine.drug_classImmunologyHuman leukocyte antigenMonoclonal antibodyBiochemistryGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineNatalizumabRheumatologymedicineAdalimumabImmunology and Allergy030203 arthritis & rheumatologyInflammationAnkylosing spondylitisBiochemistry Genetics and Molecular Biology (all)business.industryMultiple sclerosisMedicine (all)Sacroiliitismedicine.diseaseTreatmentSettore MED/16 - Reumatologia030104 developmental biologyImmunologyTumor necrosis factor alphaSpondyloarthritibusinessmedicine.drug
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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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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Innate immune response to tick-borne pathogens: Cellular and molecular mechanisms induced in the hosts

2020

This article belongs to the Special Issue Inflammasome.

0301 basic medicineInnate immune responseHost Defense MechanismReviewInflammasomelcsh:ChemistryTicksTheileriaTick borne pathogensRickettsialcsh:QH301-705.5SpectroscopyGene ontology analysisgene ontology analysisInflammasomeGeneral MedicineAcquired immune systemComputer Science ApplicationsTick-Borne DiseasesTumor necrosis factor alphamedicine.drugAnaplasma030106 microbiologyEhrlichiaBabesiaBiologyCatalysisMicrobiologyInorganic Chemistry03 medical and health sciencesAntigeninflammasomeparasitic diseasesmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyInnate immune systemOrganic Chemistrygene ontology analysibiology.organism_classificationImmunity InnateComplement systemInsect Vectors030104 developmental biologyRickettsialcsh:Biology (General)lcsh:QD1-999innate immune responsetick borne pathogens
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2017

ABSTRACTTissue immunosurveillance is an important mechanism to prevent cancer. Skin treatment with the carcinogen 7,12-dimethylbenz(a)anthracene (DMBA), followed by the tumor promoter 12-O-tetra-decanoyl-phorbol-13-acetate (TPA), is an established murine model for squamous cell carcinoma (SCC). However, the innate immunological events occurring during the initiation of chemical carcinogenesis with DMBA remain elusive. Here, we discovered that natural killer (NK) cells and Langerhans cells (LC) cooperate to impair this oncogenic process in murine skin. The depletion of NK cells or LC caused an accumulation of DNA-damaged, natural killer group 2D-ligand (NKG2D-L) expressing keratinocytes and …

0301 basic medicineInnate immune systemLymphokine-activated killer cellImmunologyDMBABiology3. Good healthCell biologyImmunosurveillance03 medical and health sciencesInterleukin 21030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesisInterleukin 12Immunology and AllergyCXCL10Tumor necrosis factor alphaOncoImmunology
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Exogenous TNFR2 activation protects from acute GvHD via host T reg cell expansion

2015

Activation of TNFR2 with a novel agonist expands T reg cells in vivo and protects allo-HCT recipients from acute GvHD while sparing antilymphoma and antiinfectious properties of transplanted donor T cells.

0301 basic medicineInterleukin 2medicine.medical_treatmentImmunologyGraft vs Host DiseaseMice Inbred Strainschemical and pharmacologic phenomenaHematopoietic stem cell transplantationBiologyT-Lymphocytes RegulatoryArticleMice03 medical and health sciencesInterleukin 21immune system diseaseshemic and lymphatic diseasesmedicineAnimalsReceptors Tumor Necrosis Factor Type IIImmunology and AllergyCytotoxic T cellddc:610Research Articlesintegumentary systemMyeloid-Derived Suppressor CellsHematopoietic Stem Cell TransplantationFOXP3hemic and immune systemsmedicine.diseaseLeukemiaddc:57030104 developmental biologysurgical procedures operativeAcute DiseaseImmunologyMyeloid-derived Suppressor CellInterleukin-2FemaleTumor necrosis factor receptor 2medicine.drug
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Biofilms of Lactobacillus plantarum and Lactobacillus fermentum: Effect on stress responses, antagonistic effects on pathogen growth and immunomodula…

2016

IF 3.682; International audience; Few studies have extensively investigated probiotic functions associated with biofilms. Here, we show that strains of Lactobacillus plantarum and Lactobacillus fermentum are able to grow as biofilm on abiotic surfaces, but the biomass density differs between strains. We performed microtiter plate biofilm assays under growth conditions mimicking to the gastrointestinal environment. Osmolarity and low concentrations of bile significantly enhanced Lactobacillus spatial organization. Two L. plantarum strains were able to form biofilms under high concentrations of bile and mucus. We used the agar well-diffusion method to show that supernatants from all Lactobaci…

0301 basic medicineLimosilactobacillus fermentum[SDV]Life Sciences [q-bio][ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionProbiotic bacteriaResistanceEscherichia-coliZebrafish modelProbioticmedicine.disease_causeMonocyteslaw.inventionIn-vitroProbioticlawLactobacillusBileVibrio-choleraeZebrafishComputingMilieux_MISCELLANEOUSbiologySalmonella entericafood and beveragesInterleukin-10Salmonella entericaSulfonic-acidLactobacillus fermentum030106 microbiologyLactic-acid bacteriaMicrobiologyMicrobiologyImmunomodulation03 medical and health sciencesAntibiosisEscherichia coliPseudomonas-aeruginosa biofilmsmedicineAnimalsHumansEscherichia coliImmunomodulatory effectsTumor Necrosis Factor-alphaProbioticsBile-salt hydrolaseCommunitiesAntibiosisBiofilmbiochemical phenomena metabolism and nutritionbiology.organism_classificationImmunity InnateCulture MediaLactobacillus biofilmsMucus030104 developmental biologyBiofilms[SDV.AEN]Life Sciences [q-bio]/Food and NutritionLactobacillus plantarumLactobacillus plantarumFood ScienceFood Microbiology
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Anti-Inflammatory Activity and Cheminformatics Analysis of New Poten t 2-Substituted 1-Methyl-5-Nitroindazolinones.

2018

After the identification of the anti-inflammatory properties of VA5-13l (2-benzyl-1- methyl-5-nitroindazolinone) in previous investigations, some of its analogous compounds were designed, synthesized and evaluated in two anti-inflammatory methods: LPS-enhanced leukocyte migration assay in zebrafish; and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse ear edema. The products evaluated (3, 6, 8, 9 and 10) showed the lower values of relative leukocyte migration at 30#181;M (0.14, 0.07, 0.10, 0.13 and 0.07, respectively), while in ear edema and myeloperoxidase activity methods, all the compounds reduced inflammation, only 4 and 16 yielded unsatisfactory results. The relationship linkin…

0301 basic medicineLipopolysaccharidesLeukocyte migrationIndazolesInformaticsStereochemistrymedicine.drug_classSubstituentNitric Oxide Synthase Type IINitric OxideAnti-inflammatory03 medical and health scienceschemistry.chemical_compoundStructure-Activity RelationshipDrug DiscoverymedicineMoietyStructure–activity relationshipAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMethyleneComputingMilieux_MISCELLANEOUSAlkylZebrafishchemistry.chemical_classificationIndazoleCyclooxygenase 2 InhibitorsDose-Response Relationship DrugMolecular StructureChemistryTumor Necrosis Factor-alphaAnti-Inflammatory Agents Non-SteroidalGeneral MedicineNitro Compounds3. Good health030104 developmental biologyCyclooxygenase 2Current topics in medicinal chemistry
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Involvement of interleukin-1 type 1 receptors in lipopolysaccharide-induced sickness responses

2017

Sickness responses to lipopolysaccharide (LPS) were examined in mice with deletion of the interleukin (IL)-1 type 1 receptor (IL-1R1). IL-1R1 knockout (1(0) mice displayed intact anorexia and HPA-axis activation to intraperitoneally injected LPS (anorexia: 10 or 120 mu g/kg; HPA-axis: 120 mu g/kg), but showed attenuated but not extinguished fever (120 g/kg). Brain PGE2 synthesis was attenuated, but Cox-2 induction remained intact. Neither the tumor necrosis factor-alpha (TNF alpha) inhibitor etanercept nor the IL -6 receptor antibody tocilizumab abolished the LPS induced fever in IL -1R1 KO mice. Deletion of IL -1R1 specifically in brain endothelial cells attenuated the LPS induced fever, b…

0301 basic medicineLipopolysaccharidesMalemedicine.medical_specialtyLipopolysaccharideFeverCell- och molekylärbiologiImmunologyHypothalamusAnorexiaEtanerceptInterleukin-1 type 1 receptor; Lipopolysaccharide; Fever; Anorexia; ACTH; Corticosterone; Endothelial cells; THF alpha; Interleukin-6; PGE(2)03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compoundEating0302 clinical medicineAdrenocorticotropic HormoneCorticosteroneInternal medicinemedicineJournal ArticleAnimalsInterleukin 6ReceptorIllness BehaviorInflammationMice KnockoutReceptors Interleukin-1 Type IbiologyEndocrine and Autonomic Systemsbusiness.industryInterleukinBrainEndothelial CellsAnorexia030104 developmental biologyEndocrinologychemistrybiology.proteinTumor necrosis factor alphaFemalemedicine.symptomInflammation MediatorsbusinessCorticosterone030217 neurology & neurosurgeryCell and Molecular Biologymedicine.drug
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