Search results for "interleukin-1"

showing 10 items of 660 documents

gd T cells condition dendritic cells in vivo for priming pulmonary CD8 T cell responses against Mycobacterium tuberculosis

2006

gammadelta T cells and dendritic cells are quickly recruited to the lungs shortly after intranasal vaccination with BCG, but the functional in vivo interplay between these two cell populations and its role in the induction of adaptive immune responses is unclear. Using TCR-deficient mice and bone marrow chimeras, we show here that gammadelta T cells provide a non-redundant early source of IFN-gamma in vivo, which enhances IL-12 production by lung dendritic cells. The in vivo-conditioned dendritic cells, in turn, prime a more efficient lung CD8 T cell response against Mycobacterium tuberculosis. Thus, strategies exploiting gammadelta T cell function and IFN-gamma production could be valuable…

MaleT cellImmunologyBiologyCD8-Positive T-LymphocytesLymphocyte ActivationInterleukin 21Interferon-gammaMiceT-Lymphocyte SubsetsmedicineImmunology and AllergyCytotoxic T cellAnimalsTuberculosisIL-2 receptorAntigen-presenting cellLungFollicular dendritic cellsReceptors Antigen T-Cell gamma-deltaDendritic CellsMycobacterium tuberculosisNatural killer T cellFlow CytometryInterleukin-12Mice Mutant StrainsMice Inbred C57BLmedicine.anatomical_structureImmunologyInterleukin 12Female
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Immuno-inflammatory activation in acute cardio-embolic strokes in comparison with other subtypes of ischaemic stroke

2009

Few studies have examined the relationship between inflammatory biomarker blood levels, cardioembolic stroke subtype and neurological deficit. So the aim of our study is to evaluate plasma levels of immuno-inflammatory variables in patients with cardio-embolic acute ischaemic stroke compared to other diagnostic subtypes and to evaluate the relationship between immuno-inflammatory variables, acute neurological deficit and brain infarct volume. One hundred twenty patients with acute ischaemic stroke and 123 controls without a diagnosis of acute ischaemic stroke were evaluated. The type of acute ischaemic stroke was classified according to the TOAST classification. We evaluated plasma levels o…

MaleTOAST Classificationmedicine.medical_specialtySettore MED/09 - Medicina InternaHeart DiseasesEmbolismInterleukin-1betaSeverity of Illness IndexBrain Ischemiacytokines stroke cardioembolicCentral nervous system diseaseBrain ischemiaDisability EvaluationPredictive Value of TestsInternal medicineSeverity of illnessmedicineHumanscardiovascular diseasesStrokeAgedAged 80 and overInterleukin-6Tumor Necrosis Factor-alphaVascular diseasebusiness.industryCerebral infarctionCase-control studyHematologyMiddle Agedmedicine.diseaseSurgeryStrokeRisk Factors inflammation cytokines Stroke Cerebral infarct cerebrovascular disease cerebrovascular accidentCase-Control StudiesLinear ModelsCardiologyFemaleSettore MED/26 - NeurologiaInflammation MediatorsbusinessBiomarkers
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Pancreatic ascites hemoglobin contributes to the systemic response in acute pancreatitis.

2015

Upon hemolysis extracellular hemoglobin causes oxidative stress and cytotoxicity due to its peroxidase activity. Extracellular hemoglobin may release free hemin, which increases vascular permeability, leukocyte recruitment, and adhesion molecule expression. Pancreatitis-associated ascitic fluid is reddish and may contain extracellular hemoglobin. Our aim has been to determine the role of extracellular hemoglobin in the local and systemic inflammatory response during severe acute pancreatitis in rats. To this end we studied taurocholate-induced necrotizing pancreatitis in rats. First, extracellular hemoglobin in ascites and plasma was quantified and the hemolytic action of ascitic fluid was …

MaleTaurocholic AcidVascular Endothelial Growth Factor Amedicine.medical_specialtyNecrosisInterleukin-1betaAbdominal FatAdipose tissueVascular permeabilityInflammationBiochemistryHemoglobinsNecrosisPhysiology (medical)Internal medicinemedicineExtracellularAnimalsAscitic FluidPeritoneal LavageRats WistarPancreasPeroxidasebusiness.industryPancreatitis Acute NecrotizingTumor Necrosis Factor-alphaAscitesmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitInterleukin-10RatsOxidative StressEndocrinologyGene Expression RegulationImmunologyPancreatitisAcute pancreatitisHemoglobinmedicine.symptombusinessFree radical biologymedicine
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Correlation of virus replication, cytokine (TNF-? and IL-1) producing cells, neuronal necrosis and inflammation after intranasal infection of mice wi…

1995

The number of TNF-alpha and IL-1 beta producing cells was investigated during the acute replication phase of herpes simplex virus (HSV) in trigeminal ganglia after intranasal infection with strains of different virulence. The highly virulent strain WAL replicated strongly and induced many cytokine producing cells early in the ganglia. The low virulent strain HFEM replicated less, only few cytokine producing cells were detected late. The thymidine-kinase negative (TK-) virus 1301 did not replicate but produced some lymphocytic inflammation. The higher the virulence of strains of HSV-1 or -2 was, the stronger was the extent of histopathological lesions; moreover, a dissociation in time betwee…

MaleTime Factorsmedicine.medical_treatmentVirulenceInflammationBiologyVirus Replicationmedicine.disease_causeHerpesviridaeVirusMiceNecrosisT-Lymphocyte SubsetsVirologymedicineAnimalsSimplexvirusAdministration IntranasalNeuronsMice Inbred BALB CTumor Necrosis Factor-alphaHerpes SimplexGeneral MedicineVirologyCytokineHerpes simplex virusTrigeminal GanglionViral replicationmedicine.symptomCD8Interleukin-1Archives of Virology
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Retinoic acid inhibits nitric oxide synthase-2 expression through the retinoic acid receptor-alpha.

2000

Retinoids are multipotent modulators of cellular functions and suppress cytokine-induced production of nitric oxide (NO) in several cell types. We have explored the mechanisms by which retinoic acid (RA) regulates NO production in rat aortic smooth muscle cells (VSMC), which express NOS2 in response to proinflammatory cytokines. RA inhibited interleukin-1beta (IL-1beta)-induced NOS2 mRNA expression and NO production. These effects were attenuated by the retinoic acid receptor (RAR) antagonist CD3106, indicating that they were mediated through retinoic acid receptors (RARs). The synthetic retinoid agonists CD336 (which specifically binds RARalpha) and CD367 (which binds all RARs) but not ago…

MaleTranscription GeneticReceptors Retinoic AcidBiophysicsRetinoic acidNitric Oxide Synthase Type IIRetinoic acid receptor betaAorta ThoracicTretinoinBiochemistryGene Expression Regulation EnzymologicMuscle Smooth VascularProinflammatory cytokineRetinoic acid-inducible orphan G protein-coupled receptorRats Sprague-Dawleychemistry.chemical_compoundparasitic diseasesAnimalsPromoter Regions GeneticMolecular BiologyCells CulturedbiologyRetinoic Acid Receptor alphaNitric oxide synthase 2Cell BiologyRetinoic acid receptor gammarespiratory systemCell biologyRatsRetinoic acid receptorKineticsBiochemistrychemistryRetinoic acid receptor alphabiology.proteinNitric Oxide SynthaseInterleukin-1Biochemical and biophysical research communications
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T helper type 17-related cytokine expression is increased in the bronchial mucosa of stable chronic obstructive pulmonary disease patients.

2009

Summary There are increased numbers of activated T lymphocytes in the bronchial mucosa of stable chronic obstructive pulmonary disease (COPD) patients. T helper type 17 (Th17) cells release interleukin (IL)-17 as their effector cytokine under the control of IL-22 and IL-23. Furthermore, Th17 numbers are increased in some chronic inflammatory conditions. To investigate the expression of interleukin (IL)-17A, IL-17F, IL-21, IL-22 and IL-23 and of retinoic orphan receptor RORC2, a marker of Th17 cells, in bronchial biopsies from patients with stable COPD of different severity compared with age-matched control subjects. The expression of IL-17A, IL-17F, IL-21, IL-22, IL-23 and RORC2 was measure…

MaleTranslational StudiesReceptors Retinoic Acidmedicine.medical_treatmentImmunologyautoimmunity bronchial biopsies emphysema neutrophilsInflammationBronchiInterleukin-23Polymerase Chain ReactionStatistics NonparametricPulmonary Disease Chronic ObstructiveAutoimmunity bronchial biopsies emphysema neutrophils pathologymedicineInterleukin 23Immunology and AllergyHumansRNA MessengerAgedDNA PrimersCOPDAnalysis of VarianceMucous MembraneReceptors Thyroid Hormonebusiness.industryInterleukinsRespiratory diseaseInterleukin-17SmokingInterleukinT-Lymphocytes Helper-InducerMiddle AgedNuclear Receptor Subfamily 1 Group F Member 3medicine.diseaseImmunohistochemistryrespiratory tract diseasesRespiratory Function TestsCytokineCase-Control StudiesImmunologyFemaleInterleukin 17medicine.symptombusinessCD8
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Interleukin-1 inhibits drinking behaviour through prostaglandins, but not by nitric oxide formation

1997

Interleukin-1 beta (IL-1 beta) causes inhibition of drinking behaviour. Moreover it induces formation of prostaglandins (PGs) and nitric oxide (NO). Both PGs and NO are able to inhibit drinking stimulated by water deprivation or by intracerebroventricular (i.c.v.) administration of angiotensin II. In this study, we studied in the preoptic area (POA) the possible role of PGs and NO in the antidipsogenic action induced by IL-1 beta. IL-1 beta was injected in the lateral cerebral ventricle (i.c.v.) (2.5, 10, 20, and 40 ng/rat) or into POA (0.625, 1.25, 2.5, and 10 ng/rat). L-arginine (12.5, 25, 50, and 100 ng/rat), the precursor of NO, or NG-nitro-L-arginine methyl ester (L-NAME) (25, 50, and …

Maleendocrine systemmedicine.medical_specialtyNitric oxide formationDose dependenceDrinking BehaviorNitric OxideGeneral Biochemistry Genetics and Molecular BiologyNitric oxideRats Sprague-Dawleychemistry.chemical_compoundInternal medicinemedicineAnimalsEnzyme InhibitorsGeneral Pharmacology Toxicology and PharmaceuticsInjections IntraventricularDrinking behaviourAspirinbiologyInterleukinGeneral MedicineAngiotensin IIRatsPreoptic areaNitric oxide synthaseNG-Nitroarginine Methyl EsterEndocrinologychemistryProstaglandinsbiology.proteinNitric Oxide SynthaseInterleukin-1
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TLR7 and TLR8 ligands and antiphospholipid antibodies show synergistic effects on the induction of IL-1beta and caspase-1 in monocytes and dendritic …

2009

TLRs represent the first line of defense against invading pathogens in the innate immune system. Certain cytokines are important mediators and essentially necessary to assure an appropriately regulated immune response. Recent data gave initial evidence that IL-1beta is one of the most relevant members of these regulating cytokines. We investigated the induction of IL-1beta production in monocytes and pDCs stimulated with ligands for TLR7 and TLR8 and with antiphospholipid antibodies (aPL). Using human monocytes and pDCs for stimulation with specific TLR7 and TLR8 ligands such as resiquimod (R848) and single stranded RNA (RNA42) as well as with a human monoclonal aPL HL5B resulted in a speci…

Malemedicine.drug_classImmunologyInterleukin-1betaCaspase 1Enzyme-Linked Immunosorbent AssayCell SeparationBiologyRegulatory Sequences Nucleic AcidMonoclonal antibodyLigandsMonocytesProinflammatory cytokinechemistry.chemical_compoundImmune systemmedicineImmunology and AllergyHumansInnate immune systemCaspase 1ImidazolesHematologyTLR7Dendritic CellsTLR8Oligonucleotides AntisenseAntiphospholipid SyndromeFlow CytometrychemistryToll-Like Receptor 7Toll-Like Receptor 8Enzyme InductionImmunologyAntibodies AntiphospholipidRNAFemaleResiquimodImmunobiology
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Involvement of endogenous nitric oxide in the inhibition by endotoxin and interleukin-1 beta of gastric acid secretion.

1994

Administration of Escherichia coli endotoxin abolished the acid secretory response induced by a bolus injection of pentagastrin in the continuously perfused stomach of the anaesthetized rat. Likewise, acid secretion stimulated by the continuous intravenous perfusion of pentagastrin was inhibited by administration of interleukin-1 beta (IL-1 beta). In both cases pretreatment with NG-nitro-L-arginine methyl ester (L-NAME) but not dexamethasone or indomethacin substantially restored the secretory responses to pentagastrin. The actions of L-NAME were reversed by the prior administration of L-arginine but not by its enantiomer D-arginine. Even though L-NAME increased blood pressure, this does no…

Malemedicine.medical_specialtyArginineIn Vitro TechniquesArginineNitric OxideNitric oxideGastric Acidchemistry.chemical_compoundInternal medicineEscherichia coliMedicineAnimalsSecretionRats WistarPhenylephrineHepatologybusiness.industryStomachdigestive oral and skin physiologyGastroenterologyInterleukinRatsPentagastrinEndotoxinsEndocrinologymedicine.anatomical_structureNG-Nitroarginine Methyl EsterchemistryGastric acidFemalePentagastrinbusinessmedicine.drugInterleukin-1Journal of gastroenterology and hepatology
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Nitric oxide mediates the inhibition by interleukin-1β of pentagastrin-stimulated rat gastric acid secretion

1993

Bolus injection of interleukin-1 beta (2 micrograms kg-1, i.v.) inhibited acid secretion induced by intravenous infusion of pentagastrin (8 micrograms kg-1 h-1) in the continuously perfused stomach of the anaesthetized rat. Administration of interleukin-1 beta did not modify mean systemic arterial blood pressure. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 2-10 mg kg-1, i.v.), but not dexamethasone (5 mg kg-1, s.c. twice over 16 h), restored the acid secretory responses to pentagastrin. The actions of L-NAME were reversed by the prior administration of L-arginine (100 mg kg-1, i.v.), but not by its enantiomer D-arginine (100 mg kg-1, i.v.). L-NAME (5 mg kg-1, i.v.) increased…

Malemedicine.medical_specialtyBlood PressureBiologyPeptide hormoneArginineNitric OxideNitric oxideGastric Acidchemistry.chemical_compoundInternal medicinemedicineAnimalsRats WistarInfusions IntravenousPhenylephrineDexamethasonePharmacologyStomachStereoisomerismRatsPentagastrinNG-Nitroarginine Methyl Estermedicine.anatomical_structureEndocrinologychemistryGastrointestinal hormoneGastric acidFemalePentagastrinResearch ArticleInterleukin-1medicine.drugBritish Journal of Pharmacology
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