Search results for "Polysaccharides"

showing 10 items of 413 documents

Plasma PLTP (phospholipid-transfer protein): an emerging role in ‘reverse lipopolysaccharide transport’ and innate immunity

2011

Plasma PLTP (phospholipid-transfer protein) is a member of the lipid transfer/LBP [LPS (lipopolysaccharide)-binding protein] family, which constitutes a superfamily of genes together with the short and long PLUNC (palate, lung and nasal epithelium clone) proteins. Although PLTP was studied initially for its involvement in the metabolism of HDL (high-density lipoproteins) and reverse cholesterol transport (i.e. the metabolic pathway through which cholesterol excess can be transported from peripheral tissues back to the liver for excretion in the bile), it displays a number of additional biological properties. In particular, PLTP can modulate the lipoprotein association and metabolism of LPS …

Lipopolysaccharidesmedicine.medical_specialtyInflammationPluncBiologyBiochemistryLipopolysaccharide transportchemistry.chemical_compoundInternal medicinePhospholipid transfer proteinmedicineAnimalsBileHumansMolecular Targeted TherapyPhospholipid Transfer ProteinsInnate immune systemCholesterolReverse cholesterol transportShock SepticImmunity InnateEndocrinologyLiverchemistrylipids (amino acids peptides and proteins)medicine.symptomMetabolic Networks and PathwaysLipoproteinBiochemical Society Transactions
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Prostaglandin E2 regulates inducible nitric oxide synthase in the murine macrophage cell line J774.

1995

We have evaluated the role of prostaglandin E2 (PGE2) in the synthesis of nitric oxide (NO) by the activation of the inducible form of nitric oxide synthase (NOS) in the murine macrophage cell line, J774, stimulated with different doses of lipopolysaccharide (LPS). The stimulation of the J774 line with suboptimal doses of LPS (0.1 microgram/mL) caused a production of endogenous PGE2 that was capable of stimulating NOS activity inducing an increase in the NO synthesis, as attested by the fact that cyclooxygenase enzyme inhibitor, indomethacin, significantly reduced NO secretion. On the contrary, a higher dose of LPS (1 microgram/mL) produced high levels of PGE2 that reduced the levels of NOS…

Lipopolysaccharidesmedicine.medical_specialtyLipopolysaccharideIndomethacinEndogenyNitric OxideBiochemistryDinoprostoneNitric oxideCell Linechemistry.chemical_compoundMiceEndocrinologyInternal medicinemedicineAnimalsProstaglandin E2biologyDose-Response Relationship DrugTumor Necrosis Factor-alphaMacrophagesMolecular biologyNitric oxide synthaseEnzyme ActivationEndocrinologychemistryEnzyme inhibitorbiology.proteinlipids (amino acids peptides and proteins)Tumor necrosis factor alphaCyclooxygenaseNitric Oxide Synthasemedicine.drugProstaglandins
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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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Sex hormones modulate inflammatory mediators produced by macrophages.

1999

Lipopolysaccharidesmedicine.medical_specialtyNitric oxide biosynthesisReceptors EstradiolNitric OxideGeneral Biochemistry Genetics and Molecular BiologyCell LineHistory and Philosophy of ScienceInternal medicinemedicineAnimalsTestosteroneReceptorEstradiolbusiness.industryTumor Necrosis Factor-alphaGeneral NeuroscienceMacrophagesTumor Necrosis Factor alpha biosynthesisAndrogen MetabolismInterleukin-10EndocrinologyCell cultureReceptors AndrogenInflammation MediatorsbusinessHormoneAnnals of the New York Academy of Sciences
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Acute exercise activates nuclear factor (NF)-kappaB signaling pathway in rat skeletal muscle.

2004

Two studies were performed to investigate the effects of an acute bout of physical exercise on the nuclear protein kappaB (NF-kappaB) signaling pathway in rat skeletal muscle. In Study 1, a group of rats (n=6) was run on the treadmill at 25 m/min, 5% grade, for 1 h or until exhaustion (Ex), and compared with a second group (n=6) injected with two doses of pyrrolidine dithiocarbamate (PDTC, 100 mg/kg, i.p.) 24 and 1 h prior to the acute exercise bout. Three additional groups of rats (n=6) were injected with either 8 mg/kg (i.p.) of lipopolysaccharide (LPS), 1 mmol/kg (i.p.) t-butylhydroperoxide (tBHP), or saline (C) and killed at resting condition. Ex rats showed higher levels of NF-kappaB b…

Lipopolysaccharidesmedicine.medical_specialtyP50PyrrolidinesElectrophoretic Mobility Shift AssayIκB kinaseBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeBiochemistryRats Sprague-Dawleychemistry.chemical_compoundPyrrolidine dithiocarbamateNF-KappaB Inhibitor alphatert-ButylhydroperoxideThiocarbamatesInternal medicinePhysical Conditioning AnimalGeneticsmedicineAnimalsMuscle SkeletalMolecular Biologychemistry.chemical_classificationReactive oxygen speciesNF-kappa BSkeletal muscleI-kappa B KinaseRatsCytosolOxidative Stressmedicine.anatomical_structureEndocrinologychemistryFemaleI-kappa B ProteinsSignal transductionOxidative stressBiotechnologySignal TransductionFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Anandamide inhibits IL-12p40 production by acting on the promoter repressor element GA-12: Possible involvement of the COX-2 metabolite prostamide E 2

2007

The eCB [endoCB (cannabinoid)] system is being considered as a novel therapeutic target for immune disorders. Cytokines of the IL-12 (interleukin-12) family have essential functions in cell-mediated immunity. In the present study, we have addressed the mechanisms of action of the eCB AEA (anandamide) on the regulation of IL-12p40 in activated microglia/macrophages. We demonstrated that AEA can inhibit the expression of p35, p19 and p40 subunits, which form the biologically-active cytokines IL-12 and IL-23 in microglia stimulated with LPS (lipopolysaccharide)/IFNγ (interferon γ). Additionally, we have provided evidence that AEA reduces the transcriptional activity of the IL-12p40 gene in LPS…

Lipopolysaccharidesmedicine.medical_specialtyPolyunsaturated Alkamidesmedicine.medical_treatmentMolecular Sequence DataRepressorArachidonic AcidsBiologyInterleukin-23BiochemistryDinoprostoneInterferon-gammaMicechemistry.chemical_compoundInternal medicinemedicineAnimalsEthanolamidePromoter Regions GeneticReceptors CannabinoidMolecular BiologyCells CulturedRegulation of gene expressionMice Inbred BALB CInterleukin-12 Subunit p40Cell BiologyAnandamideEndocannabinoid systemCell biologyProtein SubunitsEndocrinologyGene Expression RegulationchemistryCyclooxygenase 2lipids (amino acids peptides and proteins)MicrogliaCannabinoidSignal transductionEndocannabinoidsSignal TransductionProstaglandin E
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Dominant negative MORT1/FADD rescues mice from CD95 and TNF-induced liver failure

2002

Derangement of the apoptotic program is considered an important cause of liver disease. It became clear that receptor-mediated apoptosis is of specific interest in this context, and CD95 and CD120a, both members of the tumor necrosis factor (TNF) receptor superfamily, are the most prominent cell death receptors involved. The death signal is induced upon ligand binding by recruitment of caspases via the adapter molecule MORT1/FADD to the receptor and their subsequent activation. To investigate the role of MORT1/FADD in hepatocyte apoptosis, we generated transgenic mice expressing liver-specific dominant negative mutant. Mice looked grossly normal; breeding and liver development were not diff…

Lipopolysaccharidesmedicine.medical_specialtyProgrammed cell deathFas-Associated Death Domain ProteinOligonucleotidesMice TransgenicAntibodiesReceptors Tumor Necrosis FactorMiceLiver diseaseAntigens CDAlbuminsInternal medicinemedicineAnimalsfas ReceptorFADDPromoter Regions GeneticAdaptor Proteins Signal TransducingLiver injuryHepatitisMice Inbred BALB CHepatologybiologyTumor Necrosis Factor-alphamedicine.diseaseFas receptorMice Inbred C57BLEndocrinologyReceptors Tumor Necrosis Factor Type IApoptosisCaspasesbiology.proteinTumor necrosis factor alphaCarrier ProteinsLiver FailureHepatology
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Production of interleukin-6, tumor necrosis factor α and interleukin-10 in vitro correlates with the clinical immune defect in chronic hemodialysis p…

1995

Production of interleukin-6, tumor necrosis factor α and interleukin-10 in vitro correlates with the clinical immune defect in chronic hemodialysis patients. In patients with chronic renal failure alterations in monokine production are a common feature. Their clinical relevance has not yet been proven. We show here a correlation between an overproduction of interleukin-(IL)-6 and tumor necrosis factor alpha (TNFα) upon stimulation with LPS by mononuclear cells in vitro and the clinical grade of immunodeficiency found in these patients. Higher levels of IL-6 and TNFα were correlated with an immunocompromized state, that is, non-responsiveness to hepatitis B vaccination, whereas patients with…

Lipopolysaccharidesmedicine.medical_specialtyTime Factorsmedicine.medical_treatmentMolecular Sequence DataImmune systemRenal DialysisInternal medicineImmunopathologymedicineHumansInterleukin 6ImmunodeficiencyBase SequencebiologyInterleukin-6Tumor Necrosis Factor-alphabusiness.industryMonokinesVaccinationAntibodies MonoclonalHepatitis Bmedicine.diseaseRecombinant ProteinsInterleukin-10MonokineInterleukin 10CytokineEndocrinologyImmune System DiseasesNephrologyImmunologybiology.proteinTumor necrosis factor alphaOligonucleotide ProbesbusinessKidney International
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Cigarette smoke increases Toll-like receptor 4 and modifies lipopolysaccharide-mediated responses in airway epithelial cells.

2008

Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke. The main goal of this study was to explore the effects of cigarette smoke extracts (CSE) on Toll-like receptor (TLR) expression and activation in a human bronchial epithelial cell line (16-HBE). The CSE increased the expression of TLR4 and the lipopolysaccharide (LPS) binding, the nuclear factor-kappaB (NF-kappaB) activation, the release of interleukin-8 (IL-8) and the chemotactic activity toward neutrophils. It did not induce TLR2 expression or extracellular signal-regulated signal kinase 1/2 (ERK1/2) activation. The LPS increased the expression of TLR4 and induced bot…

MAPK/ERK pathwayLipopolysaccharidesLipopolysaccharideNeutrophilsImmunologyBronchiRespiratory Mucosachemistry.chemical_compoundSmokeTobaccoImmunology and AllergyHumansImmunity MucosalCell Line TransformedMitogen-Activated Protein Kinase 1Toll-like receptorMitogen-Activated Protein Kinase 3Interleukin-8NF-kappa BChemotaxisEpithelial CellsOriginal ArticlesCell biologyChemokine CXCL10Toll-Like Receptor 4TLR2Chemotaxis LeukocytechemistryImmunologyTLR4Respiratory epitheliumSignal transductionSignal TransductionImmunology
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