Search results for "interleukin-1"

showing 10 items of 660 documents

Anti-senescence and Anti-inflammatory Effects of the C-terminal Moiety of PTHrP Peptides in OA Osteoblasts.

2016

Osteoarthritis (OA) is characterized by degenerative changes in the whole joint leading to physical disability in the elderly population. This condition is associated with altered bone metabolism in subchondral areas suggesting that therapeutic strategies aimed at modifying bone cell metabolism may be of interest. We have investigated the effects of several parathyroid hormone-related protein (PTHrP)-derived peptides (1-37): (N-terminal), (107-111) and (107-139) (C-terminal) on senescence features induced by inflammatory stress in human OA osteoblasts. Incubation of these primary cells with interleukin(IL)-1β led to an increased expression of senescence markers senescence-associated-β-galac…

musculoskeletal diseases0301 basic medicineSenescenceMaleAgingmedicine.medical_specialtyInterleukin-1betaParathyroid hormoneFluorescent Antibody TechniqueReal-Time Polymerase Chain ReactionDinoprostone03 medical and health sciencesDownregulation and upregulationInternal medicineBone cellOsteoarthritismedicineHumansProstaglandin E2Cells CulturedCellular SenescenceAgedOsteoblastsParathyroid hormone-related proteinbusiness.industryInterleukin-6Tumor Necrosis Factor-alphaParathyroid Hormone-Related ProteinPeptide Fragments030104 developmental biologyEndocrinologyTumor necrosis factor alphaFemaleGeriatrics and GerontologyInflammation MediatorsbusinessCell aginghormones hormone substitutes and hormone antagonistsmedicine.drugThe journals of gerontology. Series A, Biological sciences and medical sciences
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Association of interleukin-10G microsatellite polymorphism with the susceptibility of ankylosing spondylitis

2013

Study suggests an association of IL10.G poly- morphisms with AS which might contribute to the increased or decreased susceptibility to AS. IL10.G8 and G7 microsatellites alleles appear as protective alleles against the development of AS in the German subjects investigated here. Allele IL10.G9 seems to be a risk factor for the development of AS. This protective effect of variant promoter alleles could be related to differences in IL- 10 production, which may be clinically relevant.

musculoskeletal diseasesAdultMalechemical and pharmacologic phenomenaRheumatologyimmune system diseasesparasitic diseasesmedicineHumansGenetic Predisposition to DiseaseSpondylitis AnkylosingAnkylosing spondylitisPolymorphism Geneticbusiness.industryIL10 microsatellite polymorphisms ankylosing spondylitisInterleukinhemic and immune systemsJoint boneMiddle Agedmedicine.diseaseInterleukin-10Interleukin 10ImmunologyMicrosatelliteFemalebusinessAnkylosing spondylitis; Interleukin-10; Microsatellite polymorphismsMicrosatellite RepeatsJoint Bone Spine
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Interleukin 10 polymorphisms in ankylosing spondylitis.

2003

Genetic polymorphisms of the IL10 promoter region have been implicated in many autoimmune diseases, including seronegative spondyloarthropathies. We studied three SNPs (IL10-1087, -824, and -597) and two microsatellites (IL10R and IL10G) lying within the promoter region of IL10 for association with susceptibility to and clinical manifestations of ankylosing spondylitis (AS), a common form of spondyloarthritis. Four hundred and sixty-eight individuals from 182 Finnish families affected with AS were studied. No association between individual IL10 promoter region polymorphisms or marker haplotype was observed with susceptibility to AS, but weak association was noted between the IL10-597 and -8…

musculoskeletal diseasesImmunologychemical and pharmacologic phenomenaSingle-nucleotide polymorphismBiologyPolymorphism Single Nucleotideimmune system diseasesparasitic diseasesGeneticsmedicineSNPHumansSpondylitis AnkylosingAlleleSpondylitisGenetics (clinical)AllelesGenetic associationGeneticsAnkylosing spondylitisPolymorphism GeneticHaplotypehemic and immune systemsmedicine.diseaseInterleukin-10ImmunologyBASFIMicrosatellite Repeats
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Sicilian pistachio (Pistacia vera L.) nut inhibits expression and release of inflammatory mediators and reverts the increase of paracellular permeabi…

2014

Background Dietary approaches to control inflammatory bowel diseases (IBD) may include proanthocyanidin-rich foods. Our previous research showed that a hydrophilic extract from Sicilian pistachio nut (HPE) contains sub- stantial amounts of proanthocyanidins and possesses anti- inflammatory activities. Purpose We studied the effects of HPE and of its poly- meric proanthocyanidin fraction (PPF) in a cell model that simulated some conditions of IBD, consisting of interleukin (IL)-1b-stimulated Caco-2 cells. Methods HPE was prepared by Pistacia vera L. nuts, and PPF was isolated from HPE by adsorbance chromatogra- phy. Proanthocyanidins were quantified as anthocyanidins after acidic hydrolysis.…

musculoskeletal diseasesPistachio nut Inflammation Intestinal epithelium Polyphenols Proanthocyanidinscongenital hereditary and neonatal diseases and abnormalitiesCellInterleukin-1betaAnti-Inflammatory AgentsMedicine (miscellaneous)BiologyPharmacologyPermeabilityCell membraneSettore BIO/10 - BiochimicamedicineHumansNutsProanthocyanidinsViability assayIntestinal MucosaCell ProliferationNutrition and DieteticsPistaciaInterleukin-6Interleukin-8NF-kappa BEpithelial Cellsbiology.organism_classificationIntestinal epitheliumIntestinesmedicine.anatomical_structureProanthocyanidinBiochemistryCaco-2Cyclooxygenase 2Paracellular transportPistaciaCaco-2 Cells
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A novel intrinsically disordered outer membrane lipoprotein ofAggregatibacter actinomycetemcomitansbinds various cytokines and plays a role in biofil…

2017

Intrinsically disordered proteins (IDPs) do not have a well-defined and stable 3-dimensional fold. Some IDPs can function as either transient or permanent binders of other proteins and may interact with an array of ligands by adopting different conformations. A novel outer membrane lipoprotein, bacterial interleukin receptor I (BilRI) of the opportunistic oral pathogen Aggregatibacter actinomycetemcomitans binds a key gatekeeper proinflammatory cytokine interleukin (IL)-1b. Because the amino acid sequence of the novel lipoprotein resembles that of fibrinogen binder A of Haemophilus ducreyi, BilRI could have the potential to bind other proteins, such as host matrix proteins. However, from th…

outer membrane lipoproteinsbacterial cytokine receptorbiofilm matrix composition0301 basic medicineMicrobiology (medical)Virulence FactorsLipoproteinsInterleukin-1beta030106 microbiologyImmunologyGingivaBiologyIntrinsically disordered proteinsAggregatibacter actinomycetemcomitansMicrobiologybacterial cytokine receptors03 medical and health sciencesHumansInterleukin 8Periodontal Diseasesouter membrane lipoproteinTumor Necrosis Factor-alphaInterleukin-8ta1182Biochemistry and Molecular BiologyBiofilmAggregatibacter actinomycetemcomitansReceptors Interleukin-1food and beveragesintrinsically disordered proteinbiology.organism_classificationInterleukin-10Cell biologyIntrinsically Disordered ProteinsInterleukin 10EditorialInfectious DiseasesBiochemistryBiofilmsParasitologyTumor necrosis factor alphabiofilm matrix compositionsintrinsically disordered proteinsBacterial outer membraneBiokemi och molekylärbiologiResearch PaperBacterial Outer Membrane ProteinsLipoproteinVirulence
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Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS.

2005

Phosphorylated p38 mitogen-activated protein kinase (p38MAPK), but not activated c-jun-N-terminal kinase (JNK), increases in the motor neurons of transgenic mice overexpressing ALS-linked SOD1 mutants at different stages of the disease. This effect is associated with a selective increase of phosphorylated MKK3-6, MKK4 and ASK1 and a concomitant upregulation of the TNFalpha receptors (TNFR1 and TNFR2), but not IL1beta and Fas receptors. Activation of both p38 MAPK and JNK occurs in the activated microglial cells of SOD1 mutant mice at the advanced stage of the disease; however, this effect is not accompanied by the concomitant activation of the upstream kinases ASK1 and MKK3,4,6, while both …

p38 mitogen-activated protein kinasesMAP Kinase Kinase 3Mice TransgenicMAP Kinase Kinase 6BiologyMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein KinasesReceptors Tumor Necrosis FactorCellular and Molecular NeuroscienceMiceSuperoxide Dismutase-1Downregulation and upregulationAnimalsHumansASK1RNA Messengerfas ReceptorPhosphorylationReceptorProtein kinase AMolecular BiologyP38MAPK cascadeMotor NeuronsKinaseSuperoxide DismutaseTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisJNK Mitogen-Activated Protein KinasesReceptors Interleukin-1Cell BiologyCell biologyEnzyme ActivationMice Inbred C57BLDisease Models AnimalTumor Necrosis Factor Decoy ReceptorsSpinal CordReceptors Tumor Necrosis Factor Type IDisease ProgressionTumor necrosis factor alphaSignal TransductionMolecular and cellular neurosciences
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Inhibition of Rho modulates cytokine-induced prostaglandin E2 formation in renal mesangial cells.

2003

Stimulation of rat mesangial cells for 24 h with interleukin-1β(IL-1β) plus forskolin (Fk) leads to a marked increase in prostaglandin E 2 (PGE 2 ) synthesis. This effect is further enhanced by the small G-protein Rho inhibitor toxin A. A similar increase in PGE 2 formation is obtained with Y27632, a Rho-dependent kinase inhibitor, and with lovastatin, a hydroxymethylglutaryl-coenzyme A inhibitor which depletes cells from geranylgeranyl moieties and thus blocks Rho activation. In parallel to the increased PGE 2 synthesis, a potentiation of IL-1β-induced secretory group IIA phospholipases A 2 (sPLA 2 -IIA) protein expression also occurs by Rho inhibition. However, only toxin A triggers an in…

rho GTP-Binding Proteinsmedicine.medical_treatmentBlotting WesternProstaglandinBiologyDinoprostonePhospholipases Achemistry.chemical_compoundmedicineAnimalsProstaglandin E2Molecular BiologyCells CulturedForskolinMesangial cellKinaseColforsinCell BiologyMolecular biologyGlomerular MesangiumRatsPhospholipases A2Cytokinechemistrylipids (amino acids peptides and proteins)Lovastatinmedicine.drugProstaglandin EInterleukin-1Biochimica et biophysica acta
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Ultraviolet A1 radiation induces nitric oxide synthase-2 expression in human skin endothelial cells in the absence of proinflammatory cytokines.

2001

Skin exposure to ultraviolet radiation from sunlight causes erythema and edema formation as well as inflammatory responses. As some of these ultraviolet-induced effects are potentially mediated by nitric oxide synthases, we examined the role of cytokines and ultraviolet A 1 radiation (340–400 nm) on the expression of the nitric oxide synthase-2 in endothelia of normal human skin biopsies during short-term organ culture as well as expression and activity of the nitric oxide synthase-2 in in vitro cell cultures of human dermal endothelial cells. Both, cytokine challenge (interleukin-1β + tumor necrosis factor-α + interferon-γ) but also ultraviolet A 1 exposure (50 J per cm 2 ) in the absence …

ultraviolet A1Ultraviolet Raysmedicine.medical_treatmentNitric Oxide Synthase Type IIHuman skinInflammationDermatologyBiologyBiochemistryProinflammatory cytokineNitric oxideCell Linechemistry.chemical_compoundInterferon-gammanitric oxidemedicineHumansEndotheliumPromoter Regions GeneticMolecular BiologySkinTumor Necrosis Factor-alphaNitric oxide synthase 2Cell BiologyMolecular biologynitric oxide synthase-2endothelial cellsNitric oxide synthasehealing cytokinesCytokinechemistryEnzyme InductionImmunologybiology.proteinCytokinesTumor necrosis factor alphamedicine.symptomhuman skinInflammation MediatorsNitric Oxide SynthaseInterleukin-1The Journal of investigative dermatology
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The Nasal Epithelium as a Factory for Systemic Protein Delivery

2002

We have previously shown that recombinant Sendai virus (SeV) produces efficient in vivo airway epithelial gene transfer. The ability to produce therapeutic levels of circulating proteins following noninvasive gene transfer would have widespread clinical application. Here, we compared nose, lung, and skeletal muscle for the ability to produce circulating levels of the secreted mouse antiinflammatory cytokine interleukin-10 (IL10) following SeV-mediated gene transfer. High levels of serum IL10 were obtained from each site with a potency order of lung > nose > muscle for a given viral titer. Serum levels from each site were within the likely required range for anti-inflammatory effects. The co…

virusesGenetic enhancementmedicine.medical_treatmentMucous membrane of noseSendai virus03 medical and health sciences0302 clinical medicineIn vivoDrug DiscoverymedicineGeneticsAnimalsHumansMuscle SkeletalLungMolecular BiologyNose030304 developmental biologyPharmacology0303 health sciencesLungbiologyGene Transfer TechniquesSkeletal musclerespiratory systembiology.organism_classificationSendai virus3. Good healthInterleukin-10Nasal Mucosamedicine.anatomical_structureCytokine030220 oncology & carcinogenesisImmunologyCOS CellsMolecular MedicineHeLa CellsMolecular Therapy
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Enhancement by TNF-alpha of reactivation and replication of latent herpes simplex virus from trigeminal ganglia of mice.

1995

The influence of tumor-necrosis-factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukine-1 (IL-1) and IL-3 on the in vitro reactivation frequency and replication rate of trigeminal ganglia of mice latently infected with herpes simplex virus (HSV) strain KOS was studied. It could be demonstrated that TNF-alpha and possibility GM-CSF, but not IL-1 and IL-3, enhanced the reactivation frequency and replication of HSV. Interferon alpha/beta (IFN alpha/beta) prevented reactivation and replication.

virusesmedicine.medical_treatmentHerpesvirus 1 HumanBiologymedicine.disease_causeVirus ReplicationVirusHerpesviridaeMiceInterferonVirologyAlphaherpesvirinaeChlorocebus aethiopsmedicineAnimalsHumansVero CellsMice Inbred BALB CTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating FactorInterferon-alphaGeneral MedicineInterferon-betabiology.organism_classificationVirologyIn vitroVirus LatencyCytokineHerpes simplex virusViral replicationTrigeminal GanglionInterleukin-3Virus Activationmedicine.drugInterleukin-1Archives of virology
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