Search results for "Interleukin-1 Receptor-Like 1 Protein"

showing 8 items of 8 documents

ST2 and left ventricular remodeling after ST-segment elevation myocardial infarction: A cardiac magnetic resonance study.

2018

Background: The association of soluble interleukin-1 receptor-like 1 (ST2) with left ventricular (LV) remodeling is unclear in patients with a first ST-segment elevation myocardial infarction (STEMI). The objective of this work was to assess the relationship between ST2, a marker of inflammation, and cardiac magnetic resonance (CMR) imaging-derived LV remodeling after a first STEMI. Methods: We prospectively evaluated 109 patients with a first STEMI treated with primary percutaneous coronary intervention who had ST2 assessed 24 h post-reperfusion. All patients underwent CMR imaging 1 week and 6 months after STEMI. The independent associations between ST2, LV diastolic and systolic volume in…

AdultMalemedicine.medical_specialtyCardiac magnetic resonancemedicine.medical_treatmentDiastoleMagnetic Resonance Imaging Cine030204 cardiovascular system & hematologyCohort Studies03 medical and health sciencesPercutaneous Coronary Intervention0302 clinical medicineInternal medicinemedicineHumansST segmentProspective Studiescardiovascular diseases030212 general & internal medicineMyocardial infarctionVentricular remodelingEnd-systolic volumeAgedEjection fractionVentricular Remodelingbusiness.industryLeft ventricular remodelingPercutaneous coronary interventionMiddle AgedST2medicine.diseaseInterleukin-1 Receptor-Like 1 ProteinST-segment elevation myocardial infarctioncardiovascular systemCardiologyST Elevation Myocardial InfarctionFemaleCardiology and Cardiovascular MedicinebusinessCardiac magnetic resonanceBiomarkersFollow-Up Studies
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IL-33/ST2 pathway regulates neutrophil migration and predicts outcome in patients with severe alcoholic hepatitis.

2020

Background & Aims Severe alcoholic hepatitis (SAH) is associated with a high risk of infection. The IL-33/ST2 pathway is involved in sepsis control but data regarding its role in alcohol-related liver disease (ALD) are lacking. We aimed to characterize the role of IL-33/ST2 in the polymorphonuclear neutrophils (PMNs) of patients with ALD and SAH. Methods Serum and circulating neutrophils were collected from patients with SAH, alcoholic cirrhosis and healthy controls. We quantified IL-33/ST2 pathway activity and CXCR2 at baseline and after exposure to IL-33. We also determined the migration capacity of PMNs. Results The decoy receptor of IL-33 (soluble ST2 [sST2]) was increased in SAH vs. ci…

Male0301 basic medicineAlcoholic liver diseaseCirrhosisPolymorphonuclear neutrophilsNeutrophils[SDV.MHEP.PHY] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]ApoptosisGastroenterologyReceptors Interleukin-8BLiver disease0302 clinical medicineCell MovementLiver Cirrhosis AlcoholicProspective StudiesCXC chemokine receptorsReceptorCells CulturedMigrationMiddle AgedPrognosisRecombinant Proteins3. Good healthCirrhosisAlcoholic hepatitis;Cirrhosis;Infection;Interleukin-33;Migration;Polymorphonuclear neutrophilsFemale030211 gastroenterology & hepatologyAlcoholic hepatitisInfectionSignal TransductionAdultmedicine.medical_specialtyAlcoholic hepatitisSepsis03 medical and health sciencesInternal medicinemedicine[SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]Humanscardiovascular diseasesAgedHepatologyHepatitis Alcoholicbusiness.industrymedicine.diseaseInterleukin-33Interleukin-1 Receptor-Like 1 Proteinnervous system diseasesInterleukin 33030104 developmental biologyCase-Control StudiesbusinessFollow-Up Studies
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Programming of Intestinal Epithelial Differentiation by IL-33 Derived from Pericryptal Fibroblasts in Response to Systemic Infection.

2016

SummaryThe intestinal epithelium constitutes an efficient barrier against the microbial flora. Here, we demonstrate an unexpected function of IL-33 as a regulator of epithelial barrier functions. Mice lacking IL-33 showed decreased Paneth cell numbers and lethal systemic infection in response to Salmonella typhimurium. IL-33 was produced upon microbial challenge by a distinct population of pericryptal fibroblasts neighboring the intestinal stem cell niche. IL-33 programmed the differentiation of epithelial progenitors toward secretory IEC including Paneth and goblet cells. Finally, IL-33 suppressed Notch signaling in epithelial cells and induced expression of transcription factors governing…

0301 basic medicineSalmonella typhimuriumCellular differentiationPopulationNotch signaling pathwayMice TransgenicBiologydigestive systemGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineIntestine SmallmedicineAnimalsHumansCell LineageProgenitor cellIntestinal Mucosaeducationlcsh:QH301-705.5Cell Proliferationeducation.field_of_studySalmonella Infections AnimalReceptors NotchCell growthCell DifferentiationEpithelial CellsFibroblastsInterleukin-33Intestinal epitheliumInterleukin-1 Receptor-Like 1 ProteinCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)Organ SpecificityImmunologyPaneth cellSignal transduction030215 immunologySignal TransductionCell reports
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Impact of Midregional N‐Terminal Pro–Atrial Natriuretic Peptide and Soluble Suppression of Tumorigenicity 2 Levels on Heart Rhythm in Patients Treate…

2021

Background We assessed the impact of preprocedural plasma levels of MRproANP (midregional N‐terminal pro–atrial natriuretic peptide) and sST2 (soluble suppression of tumorigenicity 2) on recurrence of atrial fibrillation (AF) at 1 year after catheter ablation of AF. Methods and Results This was a prospective, multicenter, observational study including patients undergoing catheter ablation of AF. MRproANP and sST2 were measured in a peripheral venous blood preprocedure, and MRproANP was assessed in the right and left atrial blood during ablation. The primary end point was recurrent AF between 3 and 12 months postablation, defined as a documented (>30 seconds) episode of AF, flutter, or a…

Malemedicine.medical_specialtyTime Factorsmedicine.drug_classmedicine.medical_treatmentBiorhythmCatheter ablation030204 cardiovascular system & hematologyRisk Assessment03 medical and health sciences0302 clinical medicineHeart RatePredictive Value of TestsRecurrenceRisk FactorsInternal medicinecatheter ablationAtrial FibrillationmedicineNatriuretic peptideHumansIn patientArrhythmia and Electrophysiology030212 general & internal medicineHeart AtriaProspective StudiesOriginal ResearchAgedsST2business.industryMRproANPbiomarkersAtrial fibrillationPlasma levelsMiddle Agedmedicine.diseaseInterleukin-1 Receptor-Like 1 ProteinUp-RegulationHeart RhythmTreatment OutcomePro atrial natriuretic peptideCardiologyFemaleFranceCardiology and Cardiovascular MedicinebusinessCatheter Ablation and Implantable Cardioverter-DefibrillatorAtrial Natriuretic FactorJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
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Innate immunity but not NLRP3 inflammasome activation correlates with severity of stable COPD.

2014

Background In models of COPD, environmental stressors induce innate immune responses, inflammasome activation and inflammation. However, the interaction between these responses and their role in driving pulmonary inflammation in stable COPD is unknown. Objectives To investigate the activation of innate immunity and inflammasome pathways in the bronchial mucosa and bronchoalveolar lavage (BAL) of patients with stable COPD of different severity and control healthy smokers and non-smokers. Methods Innate immune mediators (interleukin (IL)-6, IL-7, IL-10, IL-27, IL-37, thymic stromal lymphopoietin (TSLP), interferon γ and their receptors, STAT1 and pSTAT1) and inflammasome components (NLRP3, NA…

EXPRESSIONMaleINTERLEUKIN-6InflammasomesCOPD PathologyChronic Obstructive Pulmonary DiseaseRespiratory SystemImmunity NLRP3 COPDBronchiReceptors Cell SurfaceRespiratory MucosaPULMONARYInterferon-gammaPulmonary Disease Chronic ObstructiveMARKERSThymic Stromal LymphopoietinSPUTUMNLR Family Pyrin Domain-Containing 3 ProteinCytokine Receptor gp130Humans1506HMGB1 ProteinAdaptor Proteins Signal TransducingAgedScience & TechnologyRECEPTORInterleukinsSmoking1103 Clinical SciencesMiddle AgedInterleukin-1 Receptor-Like 1 ProteinImmunity InnateInnate Immunityrespiratory tract diseasesANTIINFLAMMATORY CYTOKINESTAT1 Transcription FactorCase-Control StudiesT-CELLSASTHMACytokinesFemaleCOPD Pathology Innate ImmunityCarrier ProteinsLife Sciences & BiomedicineBronchoalveolar Lavage FluidSMOKERSThorax
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IL-33/ST2 pathway drives regulatory T cell dependent suppression of liver damage upon cytomegalovirus infection.

2017

Regulatory T (Treg) cells dampen an exaggerated immune response to viral infections in order to avoid immunopathology. Cytomegaloviruses (CMVs) are herpesviruses usually causing asymptomatic infection in immunocompetent hosts and induce strong cellular immunity which provides protection against CMV disease. It remains unclear how these persistent viruses manage to avoid induction of immunopathology not only during the acute infection but also during life-long persistence and virus reactivation. This may be due to numerous viral immunoevasion strategies used to specifically modulate immune responses but also induction of Treg cells by CMV infection. Here we demonstrate that liver Treg cells …

0301 basic medicineCytomegalovirus InfectionCellular immunityViral DiseasesPhysiologyvirusesCytomegalovirusT-Lymphocytes RegulatoryMice0302 clinical medicineImmunopathologyImmune PhysiologyInterleukin-33 mouse ; mouse cytomegalovirus ; ST2 protein mouse ; T-lymphocytes regulatoryCellular typesCytotoxic T cellBiology (General)Immune ResponseImmunity CellularMice Inbred BALB CImmune cellsvirus diseasesRegulatory T cells3. Good healthmedicine.anatomical_structureInfectious DiseasesLiverCytomegalovirus InfectionsWhite blood cellsAnatomyBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.Signal TransductionResearch ArticleCell biologyBlood cellsQH301-705.5Regulatory T cellImmunologyT cellschemical and pharmacologic phenomenaCytotoxic T cellsBiologyResearch and Analysis MethodsMicrobiologyVirusCell Line03 medical and health sciencesImmune systemImmunityVirologyGeneticsmedicineAnimalsMolecular Biology TechniquesMolecular BiologyMedicine and health sciencesBiology and life sciencesBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.RC581-607Interleukin-33VirologyInterleukin-1 Receptor-Like 1 ProteinInterleukin 33Mice Inbred C57BL030104 developmental biologyAnimal cellsImmunologyParasitologyImmunologic diseases. AllergySpleen030215 immunologyCloningPLoS pathogens
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Biomarkers for characterization of heart failure - Distinction of heart failure with preserved and reduced ejection fraction.

2016

Heart failure (HF) incidence is rising worldwide and HF with preserved ejection fraction (HFpEF) represents nearly half of all cases. Treatment options are still limited in HFpEF in comparison to HF with reduced ejection fraction (HFrEF).We analyzed biomarkers in the general population to characterize HFpEF and HFrEF and defined a biomarker index to differentiate HFpEF from HFrEF. Growth differentiation factor-15 (GDF-15), soluble source of tumorigenicity 2 (sST2), C-reactive protein (CRP) and NT-proBNP were measured in 5000 individuals of the population-based Gutenberg Health Study (GHS). The median follow-up time for all-cause mortality was 7.3years with 213 events.Identification of subje…

AdultMalemedicine.medical_specialtyGrowth Differentiation Factor 15Population030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicinePredictive Value of TestsInternal medicineNatriuretic Peptide BrainmedicineHumans030212 general & internal medicineeducationAgedHeart Failureeducation.field_of_studyEjection fractionbiologybusiness.industryIncidence (epidemiology)C-reactive proteinTreatment optionsStroke VolumeMiddle Agedmedicine.diseasePrognosisInterleukin-1 Receptor-Like 1 ProteinPeptide FragmentsC-Reactive ProteinHeart failurebiology.proteinCardiologyBiomarker (medicine)FemaleGDF15Cardiology and Cardiovascular MedicinebusinessBiomarkersInternational journal of cardiology
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Mast Cells Infiltrating Inflamed or Transformed Gut Alternatively Sustain Mucosal Healing or Tumor Growth.

2015

Abstract Mast cells (MC) are immune cells located next to the intestinal epithelium with regulatory function in maintaining the homeostasis of the mucosal barrier. We have investigated MC activities in colon inflammation and cancer in mice either wild-type (WT) or MC-deficient (KitW-sh) reconstituted or not with bone marrow-derived MCs. Colitis was chemically induced with dextran sodium sulfate (DSS). Tumors were induced by administering azoxymethane (AOM) intraperitoneally before DSS. Following DSS withdrawal, KitW-sh mice showed reduced weight gain and impaired tissue repair compared with their WT littermates or KitW-sh mice reconstituted with bone marrow-derived MCs. MCs were localized i…

Cancer ResearchPathologyColorectal cancerCell CountAnimals; Animals Congenic; Azoxymethane; Carcinoma; Cell Count; Cell Transformation Neoplastic; Cells Cultured; Colitis; Colonic Neoplasms; Dextran Sulfate; Epithelial Cells; Humans; Inflammatory Bowel Diseases; Interleukin-33; Intestinal Mucosa; Mast Cells; Mice; Mice Inbred C57BL; Mice Knockout; Models Biological; Proto-Oncogene Proteins c-kit; Receptors Interleukin; Regeneration; Serine Endopeptidases; Species Specificity; Specific Pathogen-Free Organisms; Cancer Research; Oncology; Medicine (all)chemistry.chemical_compoundMiceAnimals CongenicMast CellMast CellsIntestinal MucosaCells CulturedMice KnockoutColonic NeoplasmMedicine (all)Dextran SulfateSerine EndopeptidasesColitisIntestinal epitheliumSpecific Pathogen-Free OrganismsSerine EndopeptidaseProto-Oncogene Proteins c-kitCell Transformation NeoplasticOncologyColonic Neoplasmsmedicine.symptomHumanmedicine.medical_specialtyAzoxymethaneInflammationModels BiologicalImmune systemSpecies SpecificitymedicineSpecific Pathogen-Free OrganismAnimalsHumansRegenerationColitisEpithelial CellAnimalAzoxymethanebusiness.industryInflammatory Bowel DiseaseCarcinomaEpithelial CellsReceptors Interleukinmedicine.diseaseInflammatory Bowel DiseasesInterleukin-33Interleukin-1 Receptor-Like 1 ProteinMice Inbred C57BLchemistrybusinessWound healingColitiHomeostasisCancer research
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