Search results for " inflammation"

showing 10 items of 634 documents

Chronic inflammation: A key role in degeneration of bicuspid aortic valve.

2019

Abstract Introduction Bicuspid aortic valve (BAV) is the most common congenital valvular heart defect resulting from abnormal aortic cusp formation during heart development, where two of the three normal and equal sized cusps fuse into a single large cusp resulting in a two cusps aortic valve. Over the past years, much interest has been given in understanding the pathogenesis of BAV and its complications. In this review, we focused on the role of inflammation, involved in the degeneration of BAV and the development of its complications. Role of inflammation From a pathophysiological point of view, BAV may rapidly progress into aortic stenosis (AS) and is related to aortopathy. Several histo…

0301 basic medicineAortic valveHeart Defects Congenitalmedicine.medical_specialtyBicuspid aortic valveCongenital valvular heart defectHeart Valve DiseasesInflammation030204 cardiovascular system & hematologyPathogenesis03 medical and health sciences0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseInternal medicinemedicineHumanscardiovascular diseasesEndothelial dysfunctionMolecular BiologyInflammationHeart developmentNeovascularization Pathologicbusiness.industryCalcinosisChronic inflammationAortic Valve Stenosismedicine.diseaseStenosis030104 developmental biologymedicine.anatomical_structureAortic ValveChronic Diseasecardiovascular systemCardiologyAortic valve calcificationmedicine.symptombusinessCardiology and Cardiovascular MedicineJournal of molecular and cellular cardiology
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Secretion of autoimmune antibodies in the human subcutaneous adipose tissue

2018

The adipose tissue (AT) contributes to systemic and B cell intrinsic inflammation, reduced B cell responses and secretion of autoimmune antibodies. In this study we show that adipocytes in the human obese subcutaneous AT (SAT) secrete several pro-inflammatory cytokines and chemokines, which contribute to the establishment and maintenance of local and systemic inflammation, and consequent suboptimal immune responses in obese individuals, as we have previously shown. We also show that pro-inflammatory chemokines recruit immune cells expressing the corresponding receptors to the SAT, where they also contribute to local and systemic inflammation, secreting additional pro-inflammatory mediators.…

0301 basic medicineB CellsPhysiologylcsh:MedicineAutoimmunityPathology and Laboratory MedicineSystemic inflammationWhite Blood CellsAnimal CellsImmune PhysiologyPlasma cell differentiationAdipocytesMedicine and Health Scienceslcsh:ScienceImmune ResponseConnective Tissue CellsInnate Immune SystemMultidisciplinaryT CellsBody Fluids3. Good healthBloodmedicine.anatomical_structurePhysiological ParametersConnective TissueCytokinesChemokinesCellular TypesAnatomymedicine.symptomResearch ArticleLipolysisImmune CellsImmunologySubcutaneous FatInflammationBiology03 medical and health sciencesSigns and SymptomsImmune systemAntigenDiagnostic MedicinemedicineHumansObesityAntibody-Producing CellsB cellAutoantibodiesInflammationBlood CellsTumor Necrosis Factor-alphalcsh:RBody WeightAutoantibodyBiology and Life SciencesGerminal centerCell BiologyMolecular DevelopmentOxidative StressBiological Tissue030104 developmental biologyImmune SystemImmunologylcsh:QTranscription FactorsDevelopmental BiologyPLOS ONE
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Cinnamon extract inhibits allergen-specific immune responses in human and murine allergy models.

2019

Background Ceylon cinnamon has been shown to possess anti-inflammatory properties in many diseases including allergic inflammation. Objective The aim of this study was to analyse in more detail the effects of cinnamon extract (CE) and its major compounds p-cymene and trans-cinnamaldehyde (CA) on allergen-specific immune responses in vitro and in vivo. Methods Therefore, monocyte-derived mature dendritic cells (DC) from grass or birch pollen allergic donors were pulsed with the respective allergen in the presence or absence of CE, p-cymene, CA or the solvent ethanol and co-cultured with autologous CD4+ T cells. Furthermore, basophil activation test was performed with or without CE or ethanol…

0301 basic medicineCD4-Positive T-LymphocytesHypersensitivity ImmediateAllergyCinnamomum zeylanicumOvalbuminT cellImmunologyPharmacologyImmunoglobulin Emedicine.disease_causePoaceaeAllergic inflammationDermatitis Atopic03 medical and health sciencesMice0302 clinical medicineAllergenImmune systemIn vivomedicineRespiratory HypersensitivityImmunology and AllergyAnimalsHumansAcroleinBetulaCell ProliferationPlethysmography Whole BodyMice Inbred BALB CbiologyChemistryPlant ExtractsRhinitis Allergic SeasonalDendritic Cellsmedicine.diseaseCoculture TechniquesBasophilsBasophil activationDisease Models Animal030104 developmental biologymedicine.anatomical_structure030228 respiratory systembiology.proteinCymenesCytokinesPollenClinical and experimental allergy : journal of the British Society for Allergy and Clinical ImmunologyREFERENCES
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Wheat amylase-trypsin inhibitors exacerbate intestinal and airway allergic immune responses in humanized mice.

2017

Background Amylase-trypsin inhibitors (ATIs) in wheat and related cereals are potent activators of myeloid innate immune cells via engagement of TLR4. Furthermore, ATIs have been shown to serve as adjuvants in experimental intestinal inflammatory diseases. Objective The aim of this study was to analyze whether ATIs are also modifiers of allergic inflammation. Methods Therefore, CD4 + T cells from donors sensitized to grass or birch pollen were stimulated with autologous allergen-pulsed dendritic cells in the presence or absence of ATIs or the control storage protein zein from corn. To analyze allergen-induced gut and lung inflammation, immunodeficient mice were engrafted with PBMCs from the…

0301 basic medicineCD4-Positive T-LymphocytesMaleAllergyTHP-1 Cellsmedicine.medical_treatmentImmunologyInflammationOmalizumabImmunoglobulin EAllergic inflammation03 medical and health sciencesMice0302 clinical medicineImmune systemImmunology and AllergyMedicineAnimalsHumansTriticumPlant ProteinsMice KnockoutInnate immune systembiologybusiness.industryfood and beveragesmedicine.diseaseAsthmaImmunity Innate030104 developmental biologyCytokineImmunologyAmylasesbiology.protein030211 gastroenterology & hepatologyFemalemedicine.symptombusinessTrypsin Inhibitorsmedicine.drugThe Journal of allergy and clinical immunology
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Increased expression of interleukin-22 in patients with giant cell arteritis

2017

Objectives GCA is characterized by arterial remodelling driven by inflammation. IL-22 is an attractive cytokine which acts at the crosstalk between immune and stromal cells. We hypothesized that IL-22 might be induced in GCA and might be involved in disease pathogenesis. Methods Patients subjected to temporal artery biopsies (TABs) naive from therapy were enrolled: 27 biopsy-proven GCA, 8 biopsy-negative GCA, 21 biopsy-negative non-GCA patients. Expression of IL-22 was determined in TABs by immunohystochemistry, in plasma by ELISA, in peripheral blood mononuclear cells by real-time PCR and flow cytometry. Effects of IL-22 on viability and gene expression of primary cultures obtained from TA…

0301 basic medicineCD4-Positive T-LymphocytesMalearterial remodelling; autoimmunity; giant cell arteritis; inflammation; interleukin-22; pathogenesismedicine.medical_treatmentMessengerInterleukin 220302 clinical medicineimmune system diseasesarterial remodelling; autoimmunity; giant cell arteritis; inflammation; interleukin-22; pathogenesis; Aged; Aged 80 and over; CD4-Positive T-Lymphocytes; Calcium Ionophores; Carcinogens; Case-Control Studies; Enzyme-Linked Immunosorbent Assay; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; In Vitro Techniques; Interleukins; Ionomycin; Leukocytes Mononuclear; Male; RNA Messenger; Real-Time Polymerase Chain Reaction; Temporal Arteries; Tetradecanoylphorbol Acetate80 and overLeukocytesPharmacology (medical)skin and connective tissue diseasesAged 80 and overIonomycinpathogenesisautoimmunityInterleukinFlow CytometryImmunohistochemistryTemporal ArteriesCalcium IonophoresCytokinecardiovascular systemTetradecanoylphorbol AcetateFemalemedicine.symptomgiant cell arteritiStromal cellMononuclearGiant Cell ArteritisInflammationEnzyme-Linked Immunosorbent AssayIn Vitro TechniquesReal-Time Polymerase Chain ReactionPeripheral blood mononuclear cellarterial remodelling03 medical and health sciencesRheumatologymedicineHumansViability assayRNA Messengercardiovascular diseasesAged030203 arthritis & rheumatologybusiness.industryInterleukinsinterleukin-22medicine.diseaseGiant cell arteritis030104 developmental biologyinflammationCase-Control StudiesImmunologyCarcinogensLeukocytes MononuclearRNAbusiness
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Context-Dependent Role of NF-κB Signaling in Primary Liver Cancer—from Tumor Development to Therapeutic Implications

2019

Chronic inflammatory cell death is a major risk factor for the development of diverse cancers including liver cancer. Herein, disruption of the hepatic microenvironment as well as the immune cell composition are major determinants of malignant transformation and progression in hepatocellular carcinomas (HCC). Considerable research efforts have focused on the identification of predisposing factors that promote induction of an oncogenic field effect within the inflammatory liver microenvironment. Among the most prominent factors involved in this so-called inflammation-fibrosis-cancer axis is the NF-κB pathway. The dominant role of this pathway for malignant transformation and progression…

0301 basic medicineCancer ResearchCell typechronic inflammationContext (language use)Reviewlcsh:RC254-282Malignant transformation03 medical and health sciences0302 clinical medicineImmune systemMedicinebusiness.industryhepatocarcinogenesishepatocellular carcinomalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseNf κb signaling030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomaNF-κB signalingCancer researchbusinessLiver cancerPrimary liver cancerCancers
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Bacitracin and Rutin Regulate Tissue Factor Production in Inflammatory Monocytes and Acute Myeloid Leukemia Blasts

2021

Simple Summary Aberrant tissue factor (TF) expression by transformed myeloblasts and inflammatory monocytes contributes to coagulation activation in acute myeloid leukemia (AML). TF procoagulant activity (PCA) is regulated by protein disulfide isomerase (PDI), an oxidoreductase with chaperone activity, but its specific role in AML-associated TF biology is unclear. Here, we provide novel mechanistic insights into this interrelation. We show that bacitracin and rutin, two pan-inhibitors of the PDI family, prevent lipopolysaccharide (LPS)-induced monocyte TF production under inflammatory conditions and constitutive TF expression by THP1 cells and AML blasts, thus exerting promising anticoagula…

0301 basic medicineCancer ResearchMyeloidDaunorubicinacute myeloid leukemia030204 cardiovascular system & hematologyPeripheral blood mononuclear cellArticleFlow cytometry03 medical and health sciencesTissue factor0302 clinical medicineDownregulation and upregulationhemic and lymphatic diseasesmedicinecoagulationProtein disulfide-isomeraseRC254-282medicine.diagnostic_testChemistryrutinNeoplasms. Tumors. Oncology. Including cancer and carcinogensMyeloid leukemiatissue factorprotein disulfide isomeraseMolecular biology030104 developmental biologymedicine.anatomical_structureOncologyinflammationtissue factor; protein disulfide isomerase; acute myeloid leukemia; coagulation; inflammation; rutin; monocytesmonocytesmedicine.drugCancers
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Tumor Microenvironment And Epithelial Mesenchymal Transition As Targets To Overcome Tumor Multidrug Resistance

2020

It is well established that multifactorial drug resistance hinders successful cancer treatment. Tumor cell interactions with the tumor microenvironment (TME) are crucial in epithelial-mesenchymal transition (EMT) and multidrug resistance (MDR). TME-induced factors secreted by cancer cells and cancer-associated fibroblasts (CAFs) create an inflammatory microenvironment by recruiting immune cells. CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSCs) and inflammatory tumor associated macrophages (TAMs) are main immune cell types which further enhance chronic inflammation. Chronic inflammation nurtures tumor-initiating/cancer stem-like cells (CSCs), induces both EMT and MDR leading to tumor re…

0301 basic medicineCancer Researchmedicine.medical_treatmentMultidrug resistanceTargeted therapyTargeted therapy0302 clinical medicineCancer-Associated FibroblastsNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsTumor-Associated MacrophagesTumor MicroenvironmentPharmacology (medical)HypoxiaTOR Serine-Threonine KinasesSmall moleculesChemotherapy ; Hypoxia ; Inflammation ; Microenvironment ; Multidrug resistance ; Small molecules ; Targeted therapy.Drug Resistance Multiple3. Good healthDNA DemethylationGene Expression Regulation NeoplasticInfectious DiseasesOncology030220 oncology & carcinogenesisInflammation MediatorsEpithelial-Mesenchymal TransitionStromal cellMicroenvironmentBiologyProinflammatory cytokine03 medical and health sciencesCell Line TumormedicineAnimalsHumansChemotherapyEpithelial–mesenchymal transitionPharmacologyInflammationTumor microenvironmentCancerHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseHistone Deacetylase InhibitorsMultiple drug resistanceDisease Models Animal030104 developmental biologyDrug Resistance NeoplasmCancer cellCancer research
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Palmitoylethanolamide Promotes a Proresolving Macrophage Phenotype and Attenuates Atherosclerotic Plaque Formation

2018

Objective— Palmitoylethanolamide is an endogenous fatty acid mediator that is synthetized from membrane phospholipids by N -acyl phosphatidylethanolamine phospholipase D. Its biological actions are primarily mediated by PPAR-α (peroxisome proliferator-activated receptors α) and the orphan receptor GPR55. Palmitoylethanolamide exerts potent anti-inflammatory actions but its physiological role and promise as a therapeutic agent in chronic arterial inflammation, such as atherosclerosis remain unexplored. Approach and Results— First, the polarization of mouse primary macrophages towards a proinflammatory phenotype was found to reduce N -acyl phosphatidylethanolamine phospholipase D expression …

0301 basic medicineCannabinoid receptorTime FactorsMice Knockout ApoECHOLESTEROL TRANSPORTAnti-Inflammatory AgentsPhospholipaseProto-Oncogene Maschemistry.chemical_compoundCannabinoid receptor type 2Receptors CannabinoidAortachemistry.chemical_classificationMARROW-DERIVED CELLSAPOPTOTIC CELL ACCUMULATIONPlaque AtheroscleroticCell biologymacrophagesDENSITY-LIPOPROTEIN RECEPTORPhenotypeREDUCES INFLAMMATIONCB2 RECEPTOREthanolaminesFemaleCardiology and Cardiovascular MedicineSCAVENGER RECEPTORAortic DiseasesPalmitic Acidsta3111fatty acidsCell Line03 medical and health sciencesMediatorPhagocytosisPhospholipase DAnimalsHumansScavenger receptorCANNABINOID RECEPTORPhosphatidylethanolaminePalmitoylethanolamidec-Mer Tyrosine KinaseFatty acidcholesterolta3121AmidesRatsMice Inbred C57BLDisease Models Animal030104 developmental biologychemistryinflammationRECEPTOR CLASS-BatherosclerosisCONTACT ALLERGIC DERMATITISArteriosclerosis Thrombosis and Vascular Biology
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Autophagy in the pathogenesis of ankylosing spondylitis

2016

The pathogenesis of ankylosing spondylitis (AS) is not well understood, and treatment options have met with limited success. Autophagy is a highly conserved mechanism of controlled digestion of damaged organelles within a cell. It helps in the maintenance of cellular homeostasis. The process of autophagy requires the formation of an isolation membrane. They form double-membraned vesicles called “autophagosomes” that engulf a portion of the cytoplasm. Beyond the role in maintenance of cellular homeostasis, autophagy has been demonstrated as one of the most remarkable tools employed by the host cellular defense against bacteria invasion. Autophagy also affects the immune system and thus is im…

0301 basic medicineCellAutophagy-Related ProteinsATG16L1Cellular homeostasisInflammationBiologyLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Pathogenesis03 medical and health sciencesImmune systemRheumatologyATG16L1; Autophagy; Inflammation; LRRK2; Pathogenesis; Spondyloarthritis; RheumatologyPathogenesiAutophagymedicineHomeostasisHumansSpondylitis AnkylosingATG16L1InflammationAutophagyLRRK2General MedicineCell biology030104 developmental biologymedicine.anatomical_structureCytoplasmSpondyloarthritimedicine.symptomClinical Rheumatology
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