Search results for "inflammatory cytokine"

showing 10 items of 464 documents

IL-9 and IL-13 production by activated mast cells is strongly enhanced in the presence of lipopolysaccharide: NF-kappa B is decisively involved in th…

2001

Abstract Mast cells, due to their ability to produce a large panel of mediators and cytokines, participate in a variety of processes in adaptive and innate immunity. Herein we report that in primary murine bone marrow-derived mast cells activated with ionomycin or IgE-Ag the bacterial endotoxin LPS strongly enhances the expression of IL-9 and IL-13, but not IL-4. This costimulatory effect of LPS is absent in activated mast cells derived from the LPS-hyporesponsive mouse strain BALB/c-LPSd, although in these cells the proinflammatory cytokine IL-1 can still substitute for LPS. The enhanced production of mast cell-derived IL-13 in the presence of IL-1 is a novel observation. Coactivation of m…

LipopolysaccharidesImmunologyInflammationBone Marrow CellsBiologyProinflammatory cytokinechemistry.chemical_compoundMiceMice CongenicAdjuvants ImmunologicmedicineImmunology and AllergyAnimalsMast CellsPromoter Regions GeneticCells CulturedReporter geneMice Inbred BALB CMice Inbred C3HInnate immune systemBinding SitesInterleukin-13Interleukin-9NF-kappa BNFKB1Cell biologyInterleukin 33chemistryGene Expression RegulationIonomycinInterleukin 13Immunologymedicine.symptomSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
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CD11c+ Alveolar Macrophages are a Source of IL-23 During Lipopolysaccharide-Induced Acute Lung Injury

2013

Acute lung injury (ALI) is a severe pulmonary disease causing high numbers of fatalities worldwide. Innate immune responses are an integral part of the pathophysiologic events during ALI. Interleukin 23 (IL-23) is a proinflammatory mediator known to direct the inflammatory responses in various settings of infection, autoimmunity, and cancer. Interleukin 23 has been associated with proliferation and effector functions in T(H)17 cells. Surprisingly, little is known about production of IL-23 during ALI. In this study, we found expression of mRNA for IL-23p19 to be 10-fold elevated in lung homogenates of C57BL/6 mice after lipopolysaccharide (LPS)-induced ALI. Likewise, concentrations of IL-23 …

LipopolysaccharidesMaleLipopolysaccharideAcute Lung InjuryCD11cBiologyLung injuryCritical Care and Intensive Care MedicineInterleukin-23ArticleProinflammatory cytokineMicechemistry.chemical_compoundMacrophages AlveolarmedicineAnimalsInnate immune systemmedicine.diagnostic_testrespiratory systemCD11c Antigenrespiratory tract diseasesBronchoalveolar lavagechemistryImmunologyEmergency MedicineAlveolar macrophageInterleukin 17Shock
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Hepatic over-expression of TGF-beta1 promotes LPS-induced inflammatory cytokine secretion by liver cells and endotoxemic shock.

2005

Transforming growth factor-beta (TGF-beta) is an important suppressor of inflammation. However, TGF-beta has also been found to promote secretion of inflammatory cytokines, and transgenic mice, which constitutively express TGF-beta in liver, have been found to be more susceptible to endotoxemia. To approach this apparent paradox, we investigated the role of hepatic TGF-beta1 in endotoxemia by utilising inducible TGF-beta1-transgenic mice that express TGF-beta1 under control of the C-reactive protein promoter. In contrast to non-transgenic littermates, administration of lipopolysaccharide (LPS) induced strongly increased expression of TGF-beta and acute phase proteins in the TGF-beta1-transg…

LipopolysaccharidesMalemedicine.medical_specialtyLipopolysaccharidemedicine.medical_treatmentImmunologyInflammationMice TransgenicBiologyProinflammatory cytokineTransforming Growth Factor beta1chemistry.chemical_compoundMiceImmune systemTransforming Growth Factor betaInternal medicinemedicineImmunology and AllergyAnimalsSecretionAcute-Phase ReactionCells CulturedInterleukin-6Acute-phase proteinEndotoxemiaCytokineEndocrinologychemistryHepatocytesCytokine secretionmedicine.symptomInflammation MediatorsImmunology letters
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Glucose-independent improvement of vascular dysfunction in experimental sepsis by dipeptidyl-peptidase 4 inhibition.

2012

Aims Dipeptidyl peptidase-4 (DPP-4) inhibitors are a novel class of drugs for the treatment of hyperglycaemia. Preliminary evidence suggests that their antioxidant and anti-inflammatory effects may have beneficial effects on the cardiovascular complications of diabetes. In the present study, we investigate in an experimental sepsis model whether linagliptin exerts pleiotropic vascular effects independent of its glucose-lowering properties. Methods and results Linagliptin (83 mg/kg chow for 7days) was administered in a rat model of lipopolysaccharide (LPS) (10 mg/kg, single i.p. dose/24 h)-induced sepsis. Vascular relaxation, reactive oxygen species (ROS) formation, expression of NADPH oxida…

LipopolysaccharidesMalemedicine.medical_specialtyPhysiologyNeutrophilsAdministration OralVasodilationLinagliptinBiologyLinagliptinAntioxidantsProinflammatory cytokineSepsisPhysiology (medical)Internal medicineSepsismedicineLeukocytesAnimalsHumansEndothelial dysfunctionRats WistarDipeptidyl peptidase-4Respiratory BurstDipeptidyl-Peptidase IV InhibitorsNADPH oxidasemedicine.diseaseRespiratory burstRatsVasodilationOxidative StressEndocrinologyPurinesbiology.proteinQuinazolinesCardiology and Cardiovascular MedicineDiabetic Angiopathiesmedicine.drugCardiovascular research
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The RNA binding protein tristetraprolin influences the activation state of murine dendritic cells

2010

Abstract Dendritic cells (DCs) serve to maintain peripheral tolerance under steady state conditions. Upon triggering by activation signals they initiate strong immune responses. The activation of DCs is accompanied by a rapid upregulation of proinflammatory cytokines, which were shown in other cell types to be regulated by mechanisms at the transcriptional and posttranscriptional level. Tristetraprolin (TTP), an important RNA binding protein, is involved in the regulation of mRNA stability of such cytokines. In this study we analyzed the significance of TTP for mouse DCs, which were derived from TTP −/− and WT bone marrow progenitor cells (BM-DCs). Unstimulated BM-DCs of TTP −/− mice expres…

LipopolysaccharidesRNA Stabilitymedicine.medical_treatmentT cellInterleukin-1betaImmunologychemical and pharmacologic phenomenaBiologyProinflammatory cytokineMiceTristetraprolinDownregulation and upregulationhemic and lymphatic diseasesmedicineAnimalsRNA MessengerCD40 AntigensMolecular BiologyMice KnockoutCD86Mice Inbred BALB CCD40Histocompatibility Antigens Class IIRNA-Binding ProteinsPeripheral toleranceDual Specificity Phosphatase 1hemic and immune systemsDendritic Cellsrespiratory systemUp-RegulationCell biologyCytokinemedicine.anatomical_structureImmunologybiology.proteinFemaleB7-2 AntigenProto-Oncogene Proteins c-fosCD80Molecular Immunology
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Identification and characterization of a novel Ets-2-related nuclear complex implicated in the activation of the human interleukin-12 p40 gene promot…

1997

Interleukin-12 (IL-12) is a proinflammatory cytokine produced by antigen-presenting cells in response to many microbial infections. IL-12 plays an important role in the generation of T helper type-1 cells, which favor cell-mediated immune response. IL-12 is composed of two different subunits, p40 and p35, whose expression can be regulated concomitantly or differentially. Monocytic cells, the major producers of IL-12, can be primed by interferon-gamma (IFN-gamma) to produce optimal amounts of IL-12 in response to LPS stimulation as a consequence of bacterial infection. The priming effect is exerted primarily at the transcriptional level on the p40 promoter in conjunction with the effects of …

LipopolysaccharidesTranscription GeneticSequence HomologyStimulationbiosynthesis/geneticsBiochemistryChromatography Affinitychemistry.chemical_compoundMiceAnimals Base Sequence Cell Line Cell Nucleus; metabolism Chromatography; Affinity DNA-Binding Proteins Humans Interferon-gamma; pharmacology Interleukin-12; biosynthesis/genetics Kinetics Lipopolysaccharides; pharmacology Mice Molecular Sequence Data Nuclear Proteins; isolation /&/ purification/metabolism Promoter Regions; Genetic Protein-Tyrosine Kinases; metabolism Proto-Oncogene Protein c-ets-2 Proto-Oncogene Proteins; isolation /&/ purification/metabolism Repressor Proteins Sequence Homology; Nucleic Acid Trans-Activators; isolation /&/ purification/metabolism Transcription Factors Transcription; Genetic; drug effectsPromoter Regions GeneticChromatographyNuclear ProteinsMethylationProtein-Tyrosine KinasesInterleukin-12DNA-Binding ProteinsTranscriptionMolecular Sequence DataBiologyProinflammatory cytokineCell LineProto-Oncogene Protein c-ets-2Promoter RegionsInterferon-gammaGeneticSequence Homology Nucleic AcidProto-Oncogene ProteinsAnimalsHumansMolecular BiologyTranscription factorCell NucleusMolecular massBase SequenceNucleic Acidisolation /&/ purification/metabolismPromoterCell BiologyMolecular biologyIn vitroRepressor ProteinsKineticschemistryAffinitydrug effectsTrans-ActivatorspharmacologymetabolismDNATranscription Factors
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Inflammatory Characteristics of Monocytes from Pediatric Patients with Tuberous Sclerosis.

2015

Objective  Therapeutic options for the tuberous sclerosis complex (TSC) syndrome showed varying outcomes. Malfunctional tsc1 / tsc2 genes leave mTOR uninhibited, a positive downstream modulator of the innate proinflammatory immune system, which has not yet been described in pediatric patients with TSC. Methods  Using polymerase chain reaction (PCR) gene expression levels of monocytes after cultivation with lipopolysaccharide (LPS) or with LPS + mTOR inhibitor rapamycin, patients with TSC ( n  = 16) were compared with healthy subjects ( n  = 20). Results  Compared with monocytes from healthy controls, LPS showed a more prominent gene expression pattern in patients with TSC (CCL24, CXCL10, IL…

Lipopolysaccharidescongenital hereditary and neonatal diseases and abnormalitiesLipopolysaccharideGene ExpressionMonocytesProinflammatory cytokinechemistry.chemical_compoundTuberous sclerosisTuberous SclerosisGene expressionmedicineCXCL10HumansChildInflammationSirolimusbusiness.industryTOR Serine-Threonine KinasesInfant NewbornInfantGeneral Medicinemedicine.diseasemedicine.anatomical_structureCross-Sectional StudieschemistryChild PreschoolPediatrics Perinatology and Child HealthImmunologyCytokinesNeurology (clinical)TSC1TSC2Inflammation MediatorsbusinessCCL24Immunosuppressive AgentsNeuropediatrics
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Protection by nitric oxide against liver inflammatory injury in animals carrying a nitric oxide synthase-2 transgene

2001

22 pages, 7 figures, 1 table.

Lipopolysaccharidesmedicine.medical_specialtyLipopolysaccharideTransgeneBlotting WesternNitric Oxide Synthase Type IIApoptosisGalactosamineMice TransgenicLipopolysaccharideNitric OxideBiochemistryLiver cellsProinflammatory cytokineNitric oxidechemistry.chemical_compoundMiceInternal medicineGeneticsmedicineAnimalsTransgenesPromoter Regions GeneticMolecular BiologyLiver injurybiologyTumor Necrosis Factor-alphaNF-kappa BNitric oxide synthase 2medicine.diseaseEndotoxinsEndocrinologychemistryLiverbiology.proteinTumor necrosis factor alphaNitric Oxide SynthasePhosphoenolpyruvate carboxykinaseFood DeprivationBiotechnologyInterleukin-1
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Tissue inhibitor of metalloproteinases-2 (TIMP-2) in rat liver cells is increased by lipopolysaccharide and prostaglandin E2

1995

AbstractTo explore the functional role of TIMP-2 in liver, we determined TIMP-2 mRNA levels in primary rat hepatocytes and in total rat liver. Rat hepatocytes constitutively express TIMP-2 mRNA at a low level. Incubation with dexamethasone, prostaglandin E2 and a combination of inflammatory cytokines leads to an up-regulation of TIMP-2 mRNA. In rats in vivo we found a dramatic increase of TIMP-2 expression after intraperitoneal injection of lipopolysaccharide. Compared to our previous findings on TIMP-1 we conclude that TIMP-2 mRNA expression is regulated in a distinct and partially opposite manner. Over-production of TIMP-2 could inhibit the activity of metalloproteinases and thus lead to …

Lipopolysaccharidesmedicine.medical_specialtyLipopolysaccharidemedicine.medical_treatmentInflammatory mediatorIntraperitoneal injectionBiophysicsTissue inhibitor of metalloproteinaseMatrix metalloproteinaseBiochemistryDexamethasoneDinoprostoneCell LineProinflammatory cytokineMicechemistry.chemical_compoundStructural BiologyFibrosisIn vivoInternal medicineGeneticsmedicineAnimalsHumansRNA MessengerProstaglandin E2Molecular BiologyCells CulturedTissue Inhibitor of Metalloproteinase-2ChemistryMetalloendopeptidasesProteinsExtracellular matrixCell BiologyTissue inhibitor of metalloproteinasemedicine.diseaseFibrosisRatsEndocrinologyGene Expression RegulationLiverProtein BiosynthesisCytokinesRat hepatocytemedicine.drug
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Inflammasomes in Liver Fibrosis

2017

AbstractCell death and inflammation are two central elements in the development of liver fibrosis. Inflammasomes are intracellular multiprotein complexes expressed in both hepatocytes and nonparenchymal cells in the liver that are key regulators of inflammation and cell fate. They respond to cellular danger signals by activating caspase 1, releasing the proinflammatory cytokines IL-1β and IL-18, as well as initiating a novel pathway of programmed cell death termed “pyroptosis.” These processes can initiate and perpetuate an abnormal wound-healing response with the principle cellular target being the activation of hepatic stellate cells. From the various inflammasomes, the NLRP3 inflammasome…

Liver Cirrhosis0301 basic medicinemedicine.medical_treatmentAnti-Inflammatory AgentsCaspase 1BiologyLiver transplantationProinflammatory cytokine03 medical and health sciencesLiver diseaseFibrosisNLR Family Pyrin Domain-Containing 3 ProteinPyroptosismedicineAlarminsAnimalsHumansHepatologyPyroptosisInflammasomemedicine.disease030104 developmental biologyReceptors Pattern RecognitionImmunologyHepatic stellate cellInflammation MediatorsSignal Transductionmedicine.drugSeminars in Liver Disease
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