Search results for "Interleukin 13"

showing 10 items of 23 documents

IL-13 receptor α 2: A regulator of IL-13 and IL-4 signal transduction in primary human fibroblasts

2005

Background IL-13 and IL-4 share many functional properties as a result of their use of a common receptor complex comprising IL-13 receptor α 1 (IL-13Rα1) and IL-4 receptor α (IL-4Rα). The nonsignaling receptor IL-13 receptor α 2 (IL-13Rα2) binds IL-13 with high affinity and specificity and is believed to be a decoy receptor for IL-13. Objective We sought to examine the inhibitory effects of soluble and membrane-bound IL-13Rα2 on IL-13– and IL-4–mediated effects. Methods Primary human fibroblasts were grown from endobronchial biopsy specimens obtained from volunteers. Upregulation of IL-13Rα2 mRNA was measured by means of RT-PCR, and the level of surface expression was measured by means of F…

Interleukin 2medicine.medical_specialtyReceptor complexmedicine.medical_treatmentImmunologyGene ExpressionBronchiBiologyDownregulation and upregulationInternal medicinemedicineHumansImmunology and AllergyRNA MessengerReceptorCells CulturedInterleukin-13Reverse Transcriptase Polymerase Chain ReactionReceptors Interleukin-13FibroblastsFlow CytometryUp-RegulationCell biologyEndocrinologyCytokineInterleukin 13STAT proteinInterleukin-4Signal transductionSignal Transductionmedicine.drugJournal of Allergy and Clinical Immunology
researchProduct

Production of interleukin-13 by human dendritic cells after stimulation with protein allergens is a key factor for induction of T helper 2 cytokines …

2003

Dendritic cells (DC) are able to induce not only T helper 1 (Th1) but also Th2 immune responses after stimulation with allergens. While DC-derived interleukin (IL)-12 and IL-18 are the key factors for the induction of Th1 cells, early signals being involved in Th2 differentiation are less well characterized so far. To analyse such early signals we used an antigen-specific setting with CD4+ T cells from atopic donors stimulated in the presence of autologous mature DC, which were pulsed with different allergen doses. The addition of increasing amounts of allergen during DC maturation with tumour necrosis factor-alpha, IL-1beta and prostaglandin E2 resulted in enhanced secretion of IL-6 and IL…

LipopolysaccharideImmunologyStimulationBiologyInterferon-gammachemistry.chemical_compoundTh2 CellsImmune systemHumansImmunology and AllergyCells CulturedSTAT6Interleukin-13Interleukin-6Activator (genetics)InterleukinDendritic CellsOriginal ArticlesAllergensInterleukin-12Coculture TechniquesCell biologychemistryInterleukin 13ImmunologyTrans-ActivatorsSTAT proteinCytokinesInterleukin-4STAT6 Transcription FactorImmunology
researchProduct

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)
researchProduct

Echinostoma caproni: intestinal pathology in the golden hamster, a highly compatible host, and the Wistar rat, a less compatible host.

2005

The histopathological changes induced by Echinostoma caproni (Trematoda: Echinostomatidae) in a high (golden hamster) and a low compatible host (rat) were compared at 15 and 30 days post-infection. Infection of rats was characterized by a progressive increase in erosion of villi and elevated numbers of goblet cells, which could be related to the early expulsion of the parasite in a host of low compatibility. In contrast to rats, the number of goblet cell in E. caproni-infected hamsters was low, but increased numbers of neutrophils and mesenteric inflammatory cells were observed. This indicated that local inflammatory responses in hamsters were greater than in rats. An immunohistochemical st…

MalePathologymedicine.medical_specialtyImmunologyHamsterHost-Parasite InteractionsIntestinal mucosaAntigenSpecies SpecificityCricetinaeEchinostomamedicineAnimalsIntestinal Diseases ParasiticRats WistarGoblet cellAnalysis of VarianceEchinostomiasisbiologyMesocricetusGeneral Medicinebiology.organism_classificationRatsIntestinesInfectious Diseasesmedicine.anatomical_structureAntigens HelminthImmunoglobulin GInterleukin 13ParasitologyGoblet CellsEchinostomaMesocricetusGolden hamsterExperimental parasitology
researchProduct

Echinostoma caproni (Trematoda): differential in vivo cytokine responses in high and low compatible hosts.

2011

In order to investigate the factors determining the expulsion of intestinal trematodes, we have analyzed the in vivo cytokine responses at several levels and the local responses against Echinostoma caproni (Trematoda) in two host species displaying different compatibility with the parasite. The response of the high compatible host (mice) is characterized by a mixed Th1/Th2 phenotype in the spleen, Peyer's patches and mesenteric lymph nodes. At the intestine, a marked Th1 response with a marked increase of IFN-γ together with elevated number of mucosal neutrophils and expression of induced nitric oxide synthase were observed. The responses in the host of low compatibility (rats) with the par…

Malemedicine.medical_treatmentImmunologyNitric Oxide Synthase Type IISpleenPolymerase Chain ReactionHost-Parasite InteractionsMicePeyer's PatchesRandom AllocationSpecies SpecificityIn vivoEchinostomamedicineMesenteric lymph nodesAnimalsMesenteryRNA MessengerRats WistarInterleukin 5Analysis of VarianceEchinostomiasisMice Inbred ICRbiologyGeneral Medicinebiology.organism_classificationRatsIntestinesInterleukin 10Infectious Diseasesmedicine.anatomical_structureCytokineImmunologyInterleukin 13CytokinesParasitologyLymph NodesTrematodaRNA HelminthSpleenExperimental parasitology
researchProduct

Induction of a disintegrin and metalloprotease 33 during embryonic lung development and the influence of IL-13 or maternal allergy.

2009

Background Asthma pathogenesis involves gene and environmental interactions. A disintegrin and metalloprotease 33 (ADAM33)/Adam33 is a susceptibility gene for asthma and bronchial hyperresponsiveness in human beings and mice. ADAM33 is almost exclusively expressed in mesenchymal cells, including mesenchymal progenitors in developing lungs. Objective Because maternal allergy is a risk factor for asthma, we hypothesized that an allergic environment affects ADAM33/Adam33 expression during human and mouse lung development. Methods Human embryonic/fetal lung (HEL) tissues were collected from first-trimester terminations of pregnancy. These were processed immediately or used for explant culture ±…

OvalbuminImmunologyADAM33AndrologyMiceOrgan Culture TechniquesGene interactionmedicineHypersensitivityImmunology and AllergyAnimalsHumansProtein IsoformsRNA MessengerLungFetusInterleukin-13medicine.diagnostic_testbiologyGene Expression Regulation Developmentalrespiratory tract diseasesOvalbuminADAM ProteinsBronchoalveolar lavageReal-time polymerase chain reactionInterleukin 13Immunologybiology.proteinLung morphogenesisADAM33 IL-13 Asthma AllergyThe Journal of allergy and clinical immunology
researchProduct

IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease

2011

Interleukin (IL)-22 is an effector cytokine, which acts primarily on epithelial cells in the skin, gut, liver and lung. Both pro- and anti-inflammatory properties have been reported for IL-22 depending on the tissue and disease model. In a murine model of allergic airway inflammation, we found that IL-22 is predominantly produced by innate lymphoid cells in the inflamed lungs, rather than TH cells. To determine the impact of IL-22 on airway inflammation, we used allergen-sensitized IL-22-deficient mice and found that they suffer from significantly higher airway hyperreactivity upon airway challenge. IL-22-deficiency led to increased eosinophil infiltration lymphocyte invasion and production…

PathologyPulmonologymedicine.medical_treatmentT-LymphocytesIntracellular Spacelcsh:Medicine10263 Institute of Experimental ImmunologyInterleukin 22Mice0302 clinical medicineLymphocytesPhosphorylationlcsh:ScienceLung0303 health sciencesMultidisciplinaryInterleukin-13T CellsAllergy and HypersensitivityInnate lymphoid cellInterleukinrespiratory systemInnate ImmunityRecombinant Proteins3. Good healthCytokinemedicine.anatomical_structureInterleukin 13CytokinesMedicineTumor necrosis factor alphaBiological Markersmedicine.symptomResearch ArticleSTAT3 Transcription Factormedicine.medical_specialtyImmune CellsImmunologyAntigen-Presenting CellsImmunoglobulinsInflammation610 Medicine & health1100 General Agricultural and Biological SciencesBiology03 medical and health sciences1300 General Biochemistry Genetics and Molecular BiologymedicineRespiratory HypersensitivityAnimalsBiology030304 developmental biologyInflammation1000 MultidisciplinaryTumor Necrosis Factor-alphaInterleukinslcsh:RImmunityEpithelial CellsEosinophilAllergensAsthmaImmunity Innaterespiratory tract diseasesImmune SystemImmunology570 Life sciences; biologylcsh:QImmunizationBiomarkers030215 immunology
researchProduct

Interleukin 13 (IL-13)-regulated expression of the chondroprotective metalloproteinase ADAM15 is reduced in aging cartilage

2020

Objective The adamalysin metalloproteinase 15 (ADAM15) has been shown to protect against development of osteoarthritis in mice. Here, we have investigated factors that control ADAM15 levels in cartilage. Design Secretomes from wild-type and Adam15−/− chondrocytes were compared by label-free quantitative mass spectrometry. mRNA was isolated from murine knee joints, either with or without surgical induction of osteoarthritis on male C57BL/6 mice, and the expression of Adam15 and other related genes quantified by RT-qPCR. ADAM15 in human normal and osteoarthritic cartilage was investigated similarly and by fluorescent immunohistochemistry. Cultured HTB94 chondrosarcoma cells were treated with …

Senescencemedicine.medical_specialtyADAM15medicine.medical_treatmentOsteoarthritisDiseases of the musculoskeletal systemArticleMetalloproteaseAgeSettore BIO/13 - Biologia ApplicataInternal medicineOsteoarthritismedicineddc:610MetalloproteinaseMetalloproteinaseADAM15ChemistryCartilageAutophagyGeneral Medicinemedicine.diseasemedicine.anatomical_structureEndocrinologyCytokineRC925-935IL-13Interleukin 13OsteoarthritiOsteoarthritis and Cartilage Open
researchProduct

T helper cell polarisation in coeliac disease: any (T-)bet ?

2004

Recent data strongly support the view that coeliac disease is a Th1 mediated inflammatory disease as both interferon γ production and T-bet levels in gut infiltrating cells are upregulated The puzzling observation on high interferon γ (IFN-γ) but low interleukin (IL)-12 levels in coeliac disease (CD) has resulted in questions about the underlying principles of T helper cell polarisation. In this issue of G ut ,1 the molecular basis of T helper cell polarisation in CD has been illuminated by the finding that T-bet, the master transcription factor of T helper cell type 1 (Th1) cells, is upregulated in this disease [see page 1090] . The past decade has witnessed a dramatic improvement in our p…

T cellInterleukinsGastroenterologyT helper cellCoeliac DiseaseBiologyTh1 CellsGliadinUp-RegulationInterleukin 21Celiac DiseaseInterferon-gammaImmune systemmedicine.anatomical_structureInterleukin 25ImmunologyInterleukin 13medicineCytotoxic T cellCytokinesHumansIL-2 receptorT-Box Domain ProteinsTranscription FactorsGut
researchProduct

Respiratory syncytial virus inhibits ciliagenesis in differentiated normal human bronchial epithelial cells: effectiveness of N-acetylcysteine.

2012

Persistent respiratory syncytial virus (RSV) infections have been associated with the exacerbation of chronic inflammatory diseases, including chronic obstructive pulmonary disease (COPD). This virus infects the respiratory epithelium, leading to chronic inflammation, and induces the release of mucins and the loss of cilia activity, two factors that determine mucus clearance and the increase in sputum volume. These alterations involve reactive oxygen species-dependent mechanisms. The antioxidant N-acetylcysteine (NAC) has proven useful in the management of COPD, reducing symptoms, exacerbations, and accelerated lung function decline. NAC inhibits RSV infection and mucin release in human A54…

Viral DiseasesPulmonologyChronic Obstructive Pulmonary Diseaseslcsh:MedicineMucin 5ACVirus ReplicationAcetylcysteinePulmonary Disease Chronic ObstructiveTubulinRespiratory systemlcsh:ScienceCells CulturedMultidisciplinaryInterleukin-13Microscopy VideoCell DifferentiationForkhead Transcription FactorsFree Radical Scavengersrespiratory systemHost-Pathogen InteractionLower Respiratory Tract InfectionsInfectious Diseasesmedicine.anatomical_structureInterleukin 13Medicinemedicine.symptomResearch Articlemedicine.drugDrugs and DevicesInflammationBronchiRespiratory Syncytial Virus InfectionsBiologyMicrobiologyAntiviral AgentsUpper Respiratory Tract InfectionsmedicineHumansCiliaBiologyInflammationRespiratory Syncytial Virus InfectionA549 cellMucinlcsh:RImmunityEpithelial CellsAxonemal DyneinsEpitheliumAcetylcysteineGene Expression RegulationRespiratory Syncytial Virus HumanRespiratory InfectionsImmunologyRespiratory epitheliumlcsh:QPLoS ONE
researchProduct