Search results for "interleukin-1"

showing 10 items of 660 documents

Oncogene transformation can induce tolerogenicity in murine macrophages after down-regulation of immunogenicity without altering major histocompatibi…

1993

In vitro studies on cell lines may allow analyses of the mechanisms of immunogenicity and tolerogenicity in cells. We used a model of oncogenic transformation of an established murine macrophage cell line and report here that one v-mos-transformed clone expressing unaltered high amounts of MHC class I and II antigens does not induce proliferation of unprimed T cells in primary mixed lymphocyte reactions, in sharp contrast to its non-transformed parental cells. Interestingly, this clone induces specific unresponsiveness, as revealed by the lack of responsiveness of MHC-specific T cells when subsequently exposed to the pertinent MHC alloantigens in immunogenic form but unaltered MHC-third par…

MaleLymphocyteT-LymphocytesImmunologyClone (cell biology)Down-RegulationBiologyMajor histocompatibility complexImmune toleranceCell LineMiceTransformation GeneticAntigenHistocompatibility AntigensMHC class ImedicineImmune ToleranceAnimalsRNA MessengerGenes mosMice Inbred BALB CMice Inbred C3HImmunogenicityMacrophagesGeneral MedicineCell biologyClone CellsMice Inbred C57BLmedicine.anatomical_structureCell cultureImmunologybiology.proteinFemaleLymphocyte Culture Test MixedCell DivisionInterleukin-1Scandinavian journal of immunology
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Dietary polyunsaturated fatty acids reduce retinal stress induced by an elevation of intraocular pressure in rats.

2011

International audience; N-6 and n-3 polyunsaturated fatty acids (PUFAs) have been shown to prevent tissue release of inflammatory molecules. We have shown that a combination of n-6 and n-3 PUFAs is more efficient than single supplementations on the long-term consequences of intraocular pressure elevation. We hypothesized that such an association is also more effective during early retinal stress by modifying retinal proinflammatory prostaglandin and cytokine productions. Rats were supplemented for 3 months with n-6 PUFAs, n-3 PUFAs, or both n-6 and n-3 PUFAs. After 3 months, a surgical elevation of intraocular pressure was induced. Retinal morphometry and glial cell activation were evaluate…

MaleMESH : RNA MessengerMESH: Eicosapentaenoic AcidEndocrinology Diabetes and Metabolismmedicine.medical_treatment[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionInterleukin-1betaMESH: Dietary SupplementsMESH: Rats Sprague-DawleyRats Sprague-Dawleychemistry.chemical_compound0302 clinical medicineEndocrinologyMESH: Interleukin-1betaratMESH: AnimalsProstaglandin E2Prostaglandin E1MESH : Tumor Necrosis Factor-alphaMESH : Intraocular Pressure0303 health sciencesNutrition and DieteticsMESH : RatsMESH : NeurogliaMESH: RetinaMESH: Dinoprostonepression intraoculaireMESH: AlprostadilMESH: Docosahexaenoic AcidsBiochemistryEicosapentaenoic AcidDocosahexaenoic acidlipids (amino acids peptides and proteins)MESH: NeurogliaProstaglandin D2Cell activationNeurogliaMESH : Alprostadilmedicine.drugProstaglandin Emedicine.medical_specialtyMESH : DinoprostoneMESH : Interleukin-6Docosahexaenoic AcidsMESH: RatsMESH : MaleProstaglandinBiologyMESH : Interleukin-1betaDinoprostoneRetinaMESH : Diet03 medical and health sciencesMESH: DietMESH: Intraocular PressureInternal medicinemedicineMESH : Eicosapentaenoic AcidAnimalsMESH : Dietary SupplementsRNA MessengerAlprostadilprostanoids030304 developmental biologyMESH: RNA MessengerInterleukin-6Tumor Necrosis Factor-alphadietary polyunsatured fatty acidretinal stressMESH : RetinaRetinalN-6MESH: Interleukin-6MESH : Rats Sprague-Dawleyeye diseasesMESH: MaleMESH : Docosahexaenoic AcidsDietRatsN-3EndocrinologychemistryMESH: Tumor Necrosis Factor-alphaDietary Supplements030221 ophthalmology & optometryMESH : Animalssense organs[SDV.AEN]Life Sciences [q-bio]/Food and Nutritionintraocular pressure
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Search for genetic factors associated with susceptibility to multiple sclerosis.

2006

Multiple sclerosis (MS) is a cell-mediated autoimmune disease characterized by type-1 cytokine production. Environmental and individual genetic background might influence this response particularly in cytokine gene polymorphisms. We evaluated whether polymorphisms of interleukin (IL)-10, IL-12, and tumor necrosis factor (TNF)-alpha genes, which might play a role in MS pathogenesis, are associated with MS susceptibility. Genotype frequencies for all the analyzed polymorphisms were not differently distributed between cases and controls. It is reasonable to suppose that the cytokine single-nucleotide polymorphisms (SNPs) studied must be considered against a larger genetic background involving …

MaleMultiple Sclerosismedicine.medical_treatmentSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceGene FrequencymedicineSNPHumansGenetic Predisposition to DiseaseGeneticsAutoimmune diseasePolymorphism GeneticTumor Necrosis Factor-alphaGeneral NeuroscienceMultiple sclerosisInterleukinmedicine.diseaseInterleukin-12Genotype frequencyInterleukin-10tumor necrosis factor alpha genetic polymorphism genetic susceptibility genotype heredity human major clinical studyInterleukin 10CytokineCase-Control StudiesImmunologyCytokinesFemaleDisease SusceptibilityAnnals of the New York Academy of Sciences
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Interferon-γ Induces Chronic Active Myocarditis and Cardiomyopathy in Transgenic Mice

2007

Chronic heart failure is associated with an activation of the immune system characterized among other factors by the cardiac synthesis and serum expression of proinflammatory cytokines. There is unequivocal clinical and experimental evidence that the cytokine tumor necrosis factor-alpha is involved in the development of chronic heart failure, but a putative cardiotoxic potential of the proinflammatory cytokine interferon (IFN)-gamma remains primarily unknown. To investigate this issue we analyzed the cardiac phenotype of SAP-IFN-gamma transgenic mice, which constitutively express IFN-gamma in their livers and hence exhibit high circulating serum levels of this cytokine. SAP-IFN-gamma mice s…

MaleMyocarditismedicine.medical_treatmentT-LymphocytesCardiomyopathyGene ExpressionMice Inbred StrainsMice Transgenic030204 cardiovascular system & hematologyBiologyPathology and Forensic MedicineProinflammatory cytokine03 medical and health sciencesInterferon-gammaMice0302 clinical medicinemedicineAnimalsHumansInterferon gammaIntestinal MucosaPromoter Regions Genetic030304 developmental biology0303 health sciencesCardiotoxicityReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaMacrophagesHeartDendritic Cellsmedicine.diseaseInterleukin-123. Good healthRatsIntestinesMice Inbred C57BLMyocarditisSerum Amyloid P-ComponentCytokineEchocardiographyImmunologyChronic DiseaseInterleukin 12Tumor necrosis factor alphaFemaleCardiomyopathiesmedicine.drugRegular Articles
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Expression of heme oxygenase-1 and regulation by cytokines in human osteoarthritic chondrocytes

2003

Heme oxygenase-1 (HO-1) is implicated in the protection against tissue injury. We investigated the expression of this protein in cartilage sections and chondrocytes obtained from osteoarthritic patients. HO-1 was immunodetected in preparations from cartilage and also in chondrocytes cultured in the absence of stimulation. We found that HO-1 can be modulated by cytokines since the pro-inflammatory cytokines interleukin (IL)-1beta, IL-17 and tumour necrosis factor-alpha (TNF-alpha) down-regulated this protein, whereas the anti-inflammatory cytokine IL-10 exerted the opposite effect. Our results suggest a role for HO-1 as part of protective mechanisms against tissue injury in human cartilage.

MaleNecrosismedicine.medical_treatmentBiochemistryGene Expression Regulation EnzymologicChondrocytechemistry.chemical_compoundChondrocytesOsteoarthritismedicineHumansHemeAgedPharmacologyRegulation of gene expressionbusiness.industryCartilageInterleukin-17Membrane ProteinsInterleukinInterleukin-10Cell biologyHeme oxygenasemedicine.anatomical_structureCytokinechemistryHeme Oxygenase (Decyclizing)ImmunologyCytokinesFemalemedicine.symptombusinessHeme Oxygenase-1Interleukin-1Biochemical Pharmacology
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Toll-like receptor 4 defective mice carrying point or null mutations do not show increased susceptibility toCandida albicansin a model of hematogenou…

2006

We have studied the role of TLR4 in murine defenses against Candida albicans in two TLR4-defective mouse strains: C3H/HeJ mice which have defective TLR4 signaling, and TLR4-/- knockout mice. Both TLR4-defective mice strains experimentally infected with virulent C. albicans cells showed no significant difference in survival as compared with their respective controls. Recruitment of neutrophils to the peritoneal cavity of i.p. infected mice was not affected in TLR4-/-animals, but significantly enhanced in C3H/HeJ mice, compared with their control mice. In vitro production of TNF-alpha by macrophages from both types of TLR4-defective mice, in response to yeasts and hyphae of C. albicans, was n…

MaleNeutrophilsBiologyMicrobiologyInterferon-gammaMicePeritoneal cavityCandida albicansSplenocytemedicineAnimalsPoint MutationGenetic Predisposition to DiseaseCandida albicansMice KnockoutMice Inbred C3HToll-like receptorTumor Necrosis Factor-alphaCandidiasisGeneral MedicineTh1 CellsFlow Cytometrybiology.organism_classificationInterleukin-12Corpus albicansMice Inbred C57BLToll-Like Receptor 4Infectious Diseasesmedicine.anatomical_structureKnockout mouseMacrophages PeritonealTLR4Femalelipids (amino acids peptides and proteins)Tumor necrosis factor alphaMedical Mycology
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Early and mid-term effects of obstructive apneas in myocardial injury and inflammation.

2011

Abstract Background Obstructive sleep apnea (OSA) is associated with cardiovascular disorders, but the different comorbidities in OSA patients make it difficult to know their specific effects on the development of cardiovascular injury. The aim of the present study was to investigate whether recurrent obstructive apneas could lead to myocardial injury. Methods Thirty-six male Sprague–Dawley rats (300–350 g) were either acutely (3 h) or sustainably (5 h/day, for 10 days) subjected to obstructive apneas with a pattern of 15 s each, 60 apneas/h. Corresponding control groups were formed for the acute and sustained models. To assess the induction of systemic inflammation, IL1-β was measured in p…

MaleObstructive sleep apnea Myocardial injury Inflammation Animal modelsmedicine.medical_specialtyPathologyHeart diseaseHeart DiseasesInterleukin-1betaInflammationApoptosisSettore MED/10 - Malattie Dell'Apparato RespiratorioSystemic inflammationRats Sprague-DawleyInternal medicinemedicineAnimalsInflammationSleep Apnea Obstructivebusiness.industryMyocardiumSleep apneaGeneral Medicinemedicine.diseaseRatsObstructive sleep apneaDisease Models AnimalApoptosisInitial phaseAcute DiseaseCardiologyDisease ProgressionCardiovascular Injurymedicine.symptombusinessSleep medicine
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Influence of Age on Brain Edema Formation, Secondary Brain Damage and Inflammatory Response after Brain Trauma in Mice

2012

After traumatic brain injury (TBI) elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, neuroinflammation and secondary brain damage after brain trauma in mice. Young (2 months) and old (21 months) male C57Bl6N mice were anesthetized and subjected to a controlled cortical impact injury (CCI) on the right parietal cortex. Animals of both ages were randomly assigned to 15 min, 24 h, and 72 h survival. At the end of the observation periods, contusion volume, brain water content, neurolo…

MalePathologyAgingAnatomy and PhysiologyCritical Care and Emergency MedicineMouseT-LymphocytesInterleukin-1beta610 MedizinNitric Oxide Synthase Type IISystemic inflammationMiceAnesthesiologyCell Movement610 Medical sciencesEdemaImmune PhysiologyEdemaLungNeurosurgical CareMultidisciplinaryHematologic TestsQRAging and ImmunityAnimal ModelsOrgan SizeHead Injurymedicine.anatomical_structureNeurologyNeurointensive CareCytokinesMedicinemedicine.symptomResearch Articlemedicine.medical_specialtyTraumatic brain injuryScienceImmunologyInflammationBrain damageAtrophyModel OrganismsNeurorehabilitation and TraumamedicineAnimalsRNA MessengerBiologyCerebrumNeuroinflammationInflammationLungbusiness.industryInterleukin-6Tumor Necrosis Factor-alphaImmunityWatermedicine.diseaseMice Inbred C57BLGene Expression RegulationCyclooxygenase 2Immune SystemBrain InjuriesClinical ImmunologybusinessPhysiological ProcessesPLoS ONE
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Difference in the expression of IL-9 and IL-17 correlates with different histological pattern of vascular wall injury in giant cell arteritis

2015

OBJECTIVE: GCA is a large- and medium-vessel arteritis characterized by a range of histological patterns of vascular wall injury. The aim of this study was to immunologically characterize the various histological patterns of GCA. METHODS: Thirty-five consecutive patients with biopsy-proven GCA and 15 normal controls were studied. IL-8, IL-9, IL-9R, IL-17, IL-4, TGF-β and thymic stromal lymphopoietin expression was evaluated by RT-PCR and immunohistochemistry on artery biopsy specimens. Confocal microscopy was used to characterize the phenotypes of IL-9-producing and IL-9R-expressing cells. Five additional patients who had received prednisone when the temporal artery biopsy was performed wer…

MalePathologyBiopsyT-LymphocytesSettore BIO/13 - Biologia ApplicataTransforming Growth Factor betaTh9Pharmacology (medical)Aged 80 and overMicroscopy Confocalmedicine.diagnostic_testSmall vessel vasculitisVasa vasorum vasculitiInterleukin-17vasa vasorum vasculitis Giant cell arteritiMiddle AgedTemporal Arteriesmedicine.anatomical_structurePhenotypeVasa vasorum vasculitisSmall vessel vasculitiCytokinesFemaleTh17medicine.symptomVasculitisgiant cell arteritimedicine.medical_specialtyThymic stromal lymphopoietinGiant Cell ArteritisInflammationThymic Stromal LymphopoietinRheumatologyBiopsyTh17; Th9; giant cell arteritis; small vessel vasculitis; vasa vasorum vasculitismedicineHumansInterleukin 9ArteritisGlucocorticoidsAgedbusiness.industryInterleukin-9Vascular System Injuriesmedicine.diseaseGiant cell arteritisSettore MED/16 - ReumatologiaVasa vasorumCase-Control StudiesImmunologyPrednisonebusinessBiomarkers
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Expression of Interleukin-32 in the Inflamed Arteries of Patients With Giant Cell Arteritis

2011

Objective Giant cell (temporal) arteritis (GCA) is a vasculitis that mainly affects the large and medium arteries, especially the branches of the proximal aorta. Interleukin-32 (IL-32) is a recently described Th1 proinflammatory cytokine, and is mainly induced by interferon-γ (IFNγ), IL-1β, and tumor necrosis factor α (TNFα). This study was undertaken to investigate the expression and tissue distribution of IL-32 in artery biopsy specimens from patients with GCA. Methods Quantitative gene expression analysis of IL-32, IL-1β, TNFα, IFNγ, IL-6, and IL-27 was performed in artery biopsy specimens obtained from 18 patients with GCA and 15 controls. Immunohistochemistry analysis was performed to …

MalePathologyInterleukin-1betaMessenger80 and overImmunology and AllergyPharmacology (medical)Giant Cell ArteritiAged 80 and overeducation.field_of_studyReverse Transcriptase Polymerase Chain ReactionInterleukin-17StatisticsArteriesMiddle AgedFlow CytometryImmunohistochemistryTh1 responseFemaleInterleukin 17VasculitisInterleukin-32; Giant Cell Arteritis; Th1 responsemedicine.medical_specialtyGiant Cell ArteritisImmunologyPopulationBiologyStatistics NonparametricProinflammatory cytokineInterferon-gammaRheumatologymedicine.arterymedicineHumansNonparametricRNA MessengerArteritiseducationAgedAortaAged; Aged 80 and over; Arteries; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; Interferon-gamma; Interleukin-17; Interleukin-1beta; Interleukin-6; Interleukins; Male; Middle Aged; RNA Messenger; Reverse Transcriptase Polymerase Chain Reaction; Statistics Nonparametric; Th1 Cells; Tumor Necrosis Factor-alphaInterleukin-6Tumor Necrosis Factor-alphaInterleukinsTh1 Cellsmedicine.diseaseInterleukin-32Giant cell arteritisGiant cellImmunologyRNA
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