Search results for " CYTOKINE"

showing 10 items of 602 documents

Portrait of inflammatory response to ionizing radiation treatment

2015

Ionizing radiation (IR) activates both pro-and anti-proliferative signal pathways producing an imbalance in cell fate decision. IR is able to regulate several genes and factors involved in cell-cycle progression, survival and/or cell death, DNA repair and inflammation modulating an intracellular radiation-dependent response. Radiation therapy can modulate anti-tumour immune responses, modifying tumour and its microenvironment. In this review, we report how IR could stimulate inflammatory factors to affect cell fate via multiple pathways, describing their roles on gene expression regulation, fibrosis and invasive processes. Understanding the complex relationship between IR, inflammation and …

Ionizing radiationDNA repairFibrosimedicine.medical_treatmentClinical BiochemistryInflammationReviewCell fate determinationBioinformaticsImmune systemMedicineCytokineRegulation of gene expressionInflammationInvasivenebusiness.industryCancerIonizing radiation Inflammation Cytokine Fibrosis InvasivenessCell Biologymedicine.diseaseFibrosisInvasivenessRadiation therapyCytokineCancer researchmedicine.symptombusinessJournal of Inflammation
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Cannabinoid 1 Receptors in Keratinocytes Modulate Proinflammatory Chemokine Secretion and Attenuate Contact Allergic Inflammation

2013

Abstract Epidermal keratinocytes (KCs) and cannabinoid (CB) receptors both participate in the regulation of inflammatory responses in a mouse model for allergic contact dermatitis, the contact hypersensitivity (CHS) response to the obligate sensitizer 2,4-dinitrofluorobenzene. In this study, we investigated the cellular and molecular mechanisms how CB1 receptors attenuate CHS responses to 2,4-dinitrofluorobenzene. We used a conditional gene-targeting approach to identify the relative contribution of CB1 receptors on epidermal KCs for the control of CHS responses. To determine the underlying cellular and molecular mechanisms that regulate inflammatory responses in the effector phase of CHS, …

KeratinocytesChemokineImmunologyInflammationStimulationBiologyProinflammatory cytokineAllergic inflammationInterferon-gammaMiceReceptor Cannabinoid CB1medicineAnimalsChemokine CCL8Immunology and AllergyCXCL10ReceptorCells CulturedCell ProliferationInflammationMice Knockoutintegumentary systemEarAdoptive TransferChemokine CXCL10Mice Inbred C57BLDermatitis Allergic ContactImmunologyChemokine secretionbiology.proteinDinitrofluorobenzenemedicine.symptomThe Journal of Immunology
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cFLIPL Inhibits Tumor Necrosis Factor-related Apoptosis-inducing Ligand-mediated NF-κB Activation at the Death-inducing Signaling Complex in Human Ke…

2004

Human keratinocytes undergo apoptosis following treatment with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) via surface-expressed TRAIL receptors 1 and 2. In addition, TRAIL triggers nonapoptotic signaling pathways including activation of the transcription factor NF-kappaB, in particular when TRAIL-induced apoptosis is blocked. The intracellular protein cFLIP(L) interferes with TRAIL-induced apoptosis at the death-inducing signaling complex (DISC) in many cell types. To study the role of cFLIP(L) in TRAIL signaling, we established stable HaCaT keratinocyte cell lines expressing varying levels of cFLIP(L). Functional analysis revealed that relative cFLIP(L) levels correlat…

KeratinocytesCytoplasmReceptor complexCell SurvivalCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisCell SeparationBiologyCaspase 8Sensitivity and SpecificityBiochemistryProinflammatory cytokineTNF-Related Apoptosis-Inducing LigandRibonucleasesCell Line TumorHumansEnzyme InhibitorsMolecular BiologyTranscription factorSkinInflammationCaspase 8Membrane GlycoproteinsTumor Necrosis Factor-alphaIntracellular Signaling Peptides and ProteinsNF-kappa BCell BiologyFlow CytometryRecombinant ProteinsCell biologyRetroviridaeApoptosisCaspasesDeath-inducing signaling complexRNATumor necrosis factor alphaSignal transductionApoptosis Regulatory ProteinsPropidiumProtein BindingSignal TransductionJournal of Biological Chemistry
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Induction of inflammatory cytokines in murine keratinocytes upon in vivo stimulation with contact sensitizers and tolerizing analogues

1992

In order to elucidate the role of keratinocytes (KCs) in the induction of contact sensitivity, we applied various contact sensitizers [2,4-dinitrofluorobenzene (DNFB), urushiol, 3-n-pentadecylcatechol (PDC), 4-ethoxymethylene-2-phenyloxazol-5-one (oxazolone)] and tolerizing compounds [2,4-dinitrothiocyanobenzene (DNTB), 5-methyl-3-n-pentadecyl-catechol (5-Me-PDC)] onto the earskin of non-sensitized Balb/c mice. In addition, we applied croton oil as a non-sensitizing, but stimulatory agent. Cytokine production was demonstrated by Northern blot hybridization of the total cellular RNA extracted from epidermal cells depleted by Langerhans cells and Thy 1+ dendritic cells using radiolabeled DNA …

Keratinocytesmedicine.medical_treatmentAlpha (ethology)DermatologyBiologyDermatitis ContactBiochemistryProinflammatory cytokineMiceIn vivomedicineAnimalsCroton oilRNA MessengerMicroscopy ImmunoelectronMolecular BiologyCells CulturedMice Inbred BALB CEpidermis (botany)Tumor Necrosis Factor-alphaEarBlotting NorthernImmunohistochemistryMolecular biologyStimulation ChemicalTolerance inductionCytokineImmunologyCytokinesTumor necrosis factor alphaInterleukin-1Experimental Dermatology
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OP0299 Serum and glomerular expression of IL32 in lupus nephritis

2017

Background Lupus nephritis (LN) is one of the most severe features of systemic lupus erythematosus (SLE). Several cytokines and chemokines are secreted locally in case of glomerular inflammation. Interleukin 32 (IL32) is a newly described cytokine that exhibits several properties typical of proinflammatory cytokines. Ex vivo and in vitro studies supported the role of Toll like receptors (TLRs) in LN pathogenesis and recent investigations demonstrated that Poly I:C, a ligand for (TLR) 3, strongly induced IL32 production from several cell populations. Objectives To investigate serum and urinary levels of IL32 in a cohort of LN patients compared to SLE patients without renal involvement and he…

Kidneymedicine.medical_specialtybiologybusiness.industryUrinary systemmedicine.medical_treatmentLupus nephritismedicine.diseaseProinflammatory cytokinePathogenesisInterleukin 32medicine.anatomical_structureEndocrinologyCytokineInternal medicinemedicinebiology.proteinAntibodybusinessOral Presentations
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Mucosal T cells: mediators or guardians of inflammatory bowel disease?

2003

Because the mucosal immune system is continuously exposed to a myriad of potentially harmful environmental antigens, it frequently reacts with antiinflammatory/regulatory T cell responses driven by TGF-β-producing T H 3 cells and IL-10-producing regulatory T cells. Intestinal inflammation in patients with inflammatory bowel diseases is thought to result from an overwhelming uncontrolled activation of the mucosal immune system induced by antigens of the normal luminal flora in genetically susceptible individuals. Inflammatory bowel disease appears to be mediated by subsets of CD4 + T lymphocytes or NK T cells secreting high levels of proinflammatory cytokines such as TNF-α. The increased exp…

Lamina propriaRegulatory T cellT cellGastroenterologyBiologymedicine.diseaseInflammatory bowel diseaseProinflammatory cytokinemedicine.anatomical_structureImmune systemAntigenImmunologymedicineIL-2 receptorCurrent opinion in gastroenterology
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Leptin: A pivotal mediator of intestinal inflammation in mice

2002

Abstract Background & Aims: In addition to acting as a regulator of food intake and energy expenditure, leptin can also modulate immune and inflammatory responses. The role of leptin in intestinal inflammation is the focus of the present study. Methods: Acute and chronic colitis were induced in leptin-deficient ob/ob or wild-type (WT) mice using dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS). The severity of colitis was evaluated, and possible mechanisms were studied. Results: Leptin directly stimulates intraepithelial lymphocytes (IELs) and lamina propria mononuclear cells (LPMCs). In the DSS acute model, ob/ob mice exhibited a 72% reduction of colitis severity and sp…

LeptinSTAT3 Transcription Factormedicine.medical_specialtyColonanimal diseasesdigestive systemMonocytesProinflammatory cytokineMiceReference ValuesInternal medicinemedicineAnimalsInterferon gammaLymphocytesObesityIntestinal MucosaColitisMacrophage inflammatory proteinCells CulturedLeptin DeficiencyHepatologybusiness.industryLeptinDextran SulfateGastroenterologyColitismedicine.diseasedigestive system diseasesDNA-Binding ProteinsIsoenzymesMice Inbred C57BLEndocrinologyTrinitrobenzenesulfonic AcidCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesEnzyme InductionChronic DiseaseImmunologyTrans-ActivatorsCytokinesIntraepithelial lymphocyteFemaleTumor necrosis factor alphaDisease SusceptibilityChemokinesbusinessmedicine.drugGastroenterology
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Inactivation of Socs3 in the Hypothalamus Enhances the Hindbrain Response to Endogenous Satiety Signals via Oxytocin Signaling.

2012

Leptin is an adipocyte-derived hormone that controls energy balance by acting primarily in the CNS, but its action is lost in common forms of obesity due to central leptin resistance. One potential mechanism for such leptin resistance is an increased hypothalamic expression of Suppressor of cytokine signaling 3 (Socs3), a feedback inhibitor of the Jak-Stat pathway that prevents Stat3 activation. Ample studies have confirmed the important role of Socs3 in leptin resistance and obesity. However, the degree to which Socs3 participates in the regulation of energy homeostasis in nonobese conditions remains largely undetermined. In this study, using adult mice maintained under standard diet, we d…

Leptinmedicine.medical_specialty[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT][SDV]Life Sciences [q-bio][ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionHypothalamusHindbrainSuppressor of Cytokine Signaling ProteinsBiologyOxytocinDevazepideSatiety ResponseEnergy homeostasis03 medical and health sciencesEatingMice0302 clinical medicineHormone AntagonistsInternal medicinemedicineAnimals[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]SOCS3[ SDV.OT ] Life Sciences [q-bio]/Other [q-bio.OT]ComputingMilieux_MISCELLANEOUS030304 developmental biology2. Zero hunger0303 health sciences[SDV.OT] Life Sciences [q-bio]/Other [q-bio.OT]General NeuroscienceLeptindigestive oral and skin physiologyArticlesRhombencephalonEndocrinologyOxytocinHypothalamusSuppressor of Cytokine Signaling 3 Protein[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Receptors Cholecystokinin[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC][SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryHomeostasisHormonemedicine.drugSignal Transduction
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Voluntary distance running prevents TNF-mediated liver injury in mice through alterations of the intrahepatic immune milieu

2017

AbstractPhysical activity confers a broad spectrum of health benefits. Beyond the obvious role in metabolically driven diseases, the role of physical activity in acute liver injury is poorly explored. To study the role of physical activity in acute liver injury, a novel model of voluntary distance running in mice was developed and mice were subjected to acute liver injury induced by N-galactosamine (GalN) and lipopolysaccharide (LPS). Analyses included histological stains, immunoblotting, qRT-PCR and FACS analysis. Voluntary distance running increased to an average of 10.3 km/day after a learning curve. Running lead to a decrease in the absolute numbers of intrahepatic CD4+ T and B lymphocy…

Lifestyle modification0301 basic medicineLipopolysaccharidesMaleCancer ResearchChemokineApoptosisGalactosamineLiver Function TestsAlarminsLiver injurybiologymedicine.diagnostic_testChemotaxisNF-kappa Bmedicine.anatomical_structureLiverReceptors Pattern RecognitionModels AnimalCytokinesTumor necrosis factor alphaOriginal Articlemedicine.symptomChemokinesInflammation Mediatorsmedicine.medical_specialtyImmunologyInflammationCCL2Proinflammatory cytokine03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicinePhysical Conditioning AnimalmedicineAnimalsLiver diseasesInflammationbusiness.industryTumor Necrosis Factor-alphaMonocyteBody WeightJNK Mitogen-Activated Protein KinasesCell BiologyLiver Failure Acutemedicine.diseaseEnzyme ActivationMice Inbred C57BL030104 developmental biologyEndocrinologyImmunologybiology.proteinLiver function testsbusinessCell Death & Disease
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Hop-derived fraction rich in beta acids and prenylflavonoids regulates the inflammatory response in dendritic cells differently from quercetin: unvei…

2021

Dendritic cells (DCs) represent a heterogeneous family of immune cells that link innate and adaptive immunity and their activation is linked to metabolic changes that are essential to support their activity and function. Hence, targeting the metabolism of DCs represents an opportunity to modify the inflammatory and immune response. Among the natural matrices, Humulus lupulus (Hop) compounds have recently been shown to exhibit immunomodulatory and anti-inflammatory activity. This study aimed to evaluate the ability of specific Hop fractions to modulate DCs metabolism after stimulation with lipopolysaccharide (LPS) by an untargeted metabolomics approach and compare their effect with flavonol …

LipopolysaccharideHop fractions Dendritic cells metabolomics analysis Nrf2/Nqo1 pathwayAnti-Inflammatory AgentsSuccinic AcidInbred C57BLMass SpectrometryProinflammatory cytokineHop (networking)chemistry.chemical_compoundMiceMetabolomicsImmune systemBone MarrowAnimalsMetabolomicsAnimals; Anti-Inflammatory Agents; Bone Marrow; Citrulline; Dendritic Cells; Disease Models Animal; Flavonoids; Humulus; Inflammation; Mass Spectrometry; Metabolomics; Mice; Mice Inbred C57BL; Plant Extracts; Purines; Pyrimidines; Quercetin; Succinic AcidHumulusFlavonoidsInflammationChemistryAnimalPlant ExtractsGeneral MedicineDendritic CellsAcquired immune systemSettore CHIM/08 - Chimica FarmaceuticaCell biologyMice Inbred C57BLDisease Models AnimalPyrimidinesPurinesDisease ModelsCitrullineTumor necrosis factor alphaQuercetinQuercetinFood ScienceFoodfunction
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