Search results for " peptide"

showing 10 items of 2395 documents

Neonatal NET-inhibitory factor and related peptides inhibit neutrophil extracellular trap formation.

2016

Neutrophil granulocytes, also called polymorphonuclear leukocytes (PMNs), extrude molecular lattices of decondensed chromatin studded with histones, granule enzymes, and antimicrobial peptides that are referred to as neutrophil extracellular traps (NETs). NETs capture and contain bacteria, viruses, and other pathogens. Nevertheless, experimental evidence indicates that NETs also cause inflammatory vascular and tissue damage, suggesting that identifying pathways that inhibit NET formation may have therapeutic implications. Here, we determined that neonatal NET-inhibitory factor (nNIF) is an inhibitor of NET formation in umbilical cord blood. In human neonatal and adult neutrophils, nNIF inhi…

0301 basic medicineLipopolysaccharidesMaleExtracellular TrapsNeutrophilsAntimicrobial peptidesInflammationSystemic inflammationExtracellular TrapsHistones03 medical and health sciencesmedicineAnimalsHumansCells CulturedInflammationbiologyInfant NewbornGeneral MedicineNeutrophil extracellular trapsBlood ProteinsChromatin Assembly and DisassemblyFetal BloodMolecular biologyIn vitroCell biologyNeoplasm ProteinsMice Inbred C57BLHistone citrullination030104 developmental biologyHistonebiology.proteinmedicine.symptomProtein Processing Post-TranslationalResearch ArticleThe Journal of clinical investigation
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Glucagon-like peptide-1 is associated with poor clinical outcome, lipopolysaccharide translocation and inflammation in patients undergoing cardiac su…

2020

International audience; Introduction: Cardiac surgery with cardiopulmonary bypass (CPB) is associated with gut barrier dysfunction. Gut barrier dysfunction might be estimated non-invasively by lipopolysaccharide (LPS) plasma concentration. Glucagon-like peptide-1 (GLP-1) is a gut secreted hormone that is a potential marker of mucosal integrity. Our objective was to evaluate GLP-1 as a peri-operative marker of gut barrier dysfunction in patients undergoing cardiac surgery with CPB.Methods: GLP-1, intestinal fatty acid binding protein (I-FABP) and lipopolysaccharide were assayed: at induction, after CPB and 24 h after admission in the intensive care unit. The primary end-point was peri-operat…

0301 basic medicineLipopolysaccharidesMaleLipopolysaccharideBiochemistryGastroenterologylaw.inventionchemistry.chemical_compound0302 clinical medicinelawGlucagon-Like Peptide 1Gut barrierImmunology and AllergyProspective StudiesCardiopulmonary Bypassdigestive oral and skin physiologyHematologyCardiac surgeryMiddle AgedCardiopulmonary by passIntensive care unitGlucagon-like peptide-1Digestive translocation3. Good healthCardiac surgeryGlucagon like peptid 1030220 oncology & carcinogenesisFemalemedicine.symptommedicine.medical_specialtyImmunologyInflammationLipopolysaccharide03 medical and health sciencesInternal medicineIntensive caremedicineCardiopulmonary bypassHumansCardiac Surgical ProceduresMolecular BiologyAgedInflammationbusiness.industryEndotoxemia030104 developmental biologychemistrybusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyBiomarkersHormoneCytokine
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Stress and immune response to bacterial LPS in the sea urchin Paracentrotus lividus (Lamarck, 1816).

2018

The immune system of the sea urchin species Paracentrotus lividus is highly complex and, as yet, poorly understood. P. lividus coelomocytes mediate immune response through phagocytosis and encapsulation of non-self particles, in addition to the production of antimicrobial molecules. Despite this understanding, details of exactly how these processes occur and the mechanisms which drive them are still in need of clarification. In this study, we show how the bacterial lipopolysaccharides (LPS) is able to induce a stress response which increases the levels of the heat shock proteins HSP70 and HSP90 only a few hours after treatment. This study also shows that LPS treatment increases the expressi…

0301 basic medicineLipopolysaccharidesPhagocytosisAntimicrobial peptidesAquatic ScienceParacentrotus lividusAntimicrobical peptide03 medical and health sciencesImmune systemStress PhysiologicalHeat shock proteinbiology.animalEnvironmental ChemistryHSP90AnimalsSea urchinHSP70Heat-Shock ProteinsbiologyEchinoderm04 agricultural and veterinary sciencesGeneral Medicinebiology.organism_classificationHsp90Immunity InnateHsp70Cell biologyThymosin030104 developmental biologyImmune System040102 fisheriesbiology.proteinParacentrotus0401 agriculture forestry and fisheriesCoelomocyteParacentrotus lividuFishshellfish immunology
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Ceftaroline modulates the innate immune and host defense responses of immunocompetent cells exposed to cigarette smoke.

2017

Abstract Background Cigarette smoke, the principal risk factor for chronic obstructive pulmonary disease (COPD), negatively influences the effectiveness of the immune system’s response to a pathogen. The antibiotic ceftaroline exerts immune-modulatory effects in bronchial epithelial cells exposed to cigarette smoke. Aims and methods The present study aims to assess the effects of ceftaroline on TLR2 and TLR4 expression, LPS binding and TNF-α and human beta defensin (HBD2) release in an undifferentiated and PMA-differentiated human monocyte cell line (THP-1) exposed or not to cigarette smoke extracts (CSE). TLR2, TLR4, and LPS binding were assessed by flow cytometry, TNF-α and HBD2 release w…

0301 basic medicineLipopolysaccharidesbeta-DefensinsCell SurvivalCephalosporinLipopolysaccharideToxicologyMonocytes03 medical and health sciencesImmunologic Factor0302 clinical medicineImmune systemCell Line TumorSmokeAnti-Bacterial AgentmedicineHumansImmunologic FactorsInnate immune systemImmunocompetent cellDose-Response Relationship Drugbusiness.industryTumor Necrosis Factor-alphaMonocyteMacrophagesSmokingAntibioticCigarette smokeGeneral MedicineImmunity InnateToll-Like Receptor 2Anti-Bacterial AgentsCephalosporinsHost-Pathogen InteractionToll-Like Receptor 4TLR2030104 developmental biologymedicine.anatomical_structureBeta defensinCell cultureImmunologyHost-Pathogen InteractionsTLR4lipids (amino acids peptides and proteins)Tumor necrosis factor alphabusinessImmunocompetence030215 immunologyToxicology letters
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Amyloid β-peptide insertion in liposomes containing GM1-cholesterol domains.

2015

Neuronal membrane damage is related to the early impairments appearing in Alzheimer's disease due to the interaction of the amyloid β-peptide (Aβ) with the phospholipid bilayer. In particular, the ganglioside GM1, present with cholesterol in lipid rafts, seems to be able to initiate Aβ aggregation on membrane. We studied the thermodynamic and structural effects of the presence of GM1 on the interaction between Aβ and liposomes, a good membrane model system. Isothermal Titration Calorimetry highlighted the importance of the presence of GM1 in recruiting monomeric Aβ toward the lipid bilayer. Light and Small Angle X-ray Scattering revealed a different pattern for GM1 containing liposomes, bot…

0301 basic medicineLiposomeGangliosideAmyloid beta-PeptidesAmyloidCalorimetry Differential ScanningChemistryBilayerOrganic ChemistryBiophysicsIsothermal titration calorimetryG(M1) GangliosideBiochemistry03 medical and health sciences030104 developmental biologyMembraneCholesterolBiochemistryLiposomesThermodynamicslipids (amino acids peptides and proteins)A?-membrane interaction; Double layer perturbation; Isothermal titration calorimetry; Small angle X-ray scatteringLipid bilayerLipid raftBiophysical chemistry
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Molecular mechanisms underlying the neuroprotective role of atrial natriuretic peptide in experimental acute ischemic stroke

2018

Abstract Along with its role in regulating blood pressure and fluid homeostasis, the natriuretic peptide system could be also part of an endogenous protective mechanism against brain damage. We aimed to assess the possibility that exogenous atrial natriuretic peptide (ANP) could protect against acute ischemic stroke, as well as the molecular mechanisms involved. Three groups of rats subjected to transient middle cerebral artery occlusion (tMCAO, intraluminal filament technique, 60 min) received intracerebroventricular vehicle, low-dose ANP (0.5 nmol) or high-dose ANP (2.5 nmol), at 30 min reperfusion. Neurofunctional condition, and brain infarct and edema volumes were measured at 24 h after…

0301 basic medicineMAPK/ERK pathwayMalePotassium ChannelsSignaling pathwaysmedicine.drug_classMAP Kinase Signaling SystemAcute ischemic strokeDown-RegulationApoptosisBrain damagePharmacologyBiochemistryNeuroprotectionBrain Ischemia03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineEndocrinologyAtrial natriuretic peptideNatriuretic peptideMedicineAnimalsDNA CleavageRats WistarReceptorAtrial natriuretic peptideMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayInjections Intraventricularbusiness.industryCaspase 3Natriuretic peptide receptorsBrainInfarction Middle Cerebral ArteryStroke030104 developmental biologyNeuroprotective AgentsReperfusion InjuryK+ channelsmedicine.symptombusinessProto-Oncogene Proteins c-aktReceptors Atrial Natriuretic Factor030217 neurology & neurosurgeryAtrial Natriuretic Factorhormones hormone substitutes and hormone antagonists
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The Role of ERK Signaling in Experimental Autoimmune Encephalomyelitis

2017

Extracellular signal-regulated kinase (ERK) signaling plays a crucial role in regulating immune cell function and has been implicated in autoimmune disorders. To date, all commercially available inhibitors of ERK target upstream components, such as mitogen-activated protein (MAP) kinase/ERK kinase (MEKs), but not ERK itself. Here, we directly inhibit nuclear ERK translocation by a novel pharmacological approach (Glu-Pro-Glu (EPE) peptide), leading to an increase in cytosolic ERK phosphorylation during T helper (Th)17 cell differentiation. This was accompanied by diminished secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine influencing the encephalitogenicity …

0301 basic medicineMAPK/ERK pathwaymedicine.medical_treatmentCellular differentiationexperimental autoimmune encephalomyelitisLymphocyte Activationmedicine.disease_causemultiple sclerosisAutoimmunitylcsh:ChemistryMice0302 clinical medicineT-Lymphocyte SubsetsPhosphorylationExtracellular Signal-Regulated MAP Kinaseslcsh:QH301-705.5SpectroscopyKinaseExperimental autoimmune encephalomyelitisInterleukinGeneral MedicineComputer Science ApplicationsCell biologyProtein TransportCytokine030220 oncology & carcinogenesisFemaleERK pathwayCell signalingEncephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemT cellsBiologyModels BiologicalArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalscell signalingPhysical and Theoretical ChemistryEPE peptideMolecular BiologyT cells; ERK pathway; EPE peptide; experimental autoimmune encephalomyelitis; multiple sclerosis; cell signalingOrganic ChemistryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Th17 CellsInternational Journal of Molecular Sciences
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Negatively Charged Gangliosides Promote Membrane Association of Amphipathic Neurotransmitters

2018

Lipophilic neurotransmitters (NTs) such as dopamine are chemical messengers enabling neurotransmission by adhering onto the extracellular surface of the post-synaptic membrane in a synapse, followed by binding to their receptors. Previous studies have shown that the strength of the NT-membrane association is dependent on the lipid composition of the membrane. Negatively charged lipids such as phosphatidylserine, phosphatidylglycerol, and phosphatidic acid have been indicated to promote NT-membrane binding, however these anionic lipids reside almost exclusively in the intracellular leaflet of the post-synaptic membrane instead of the extracellular leaflet facing the synaptic cleft. Meanwhile…

0301 basic medicineMOLECULAR-DYNAMICS SIMULATIONSBIOMOLECULAR SYSTEMSkolesteroliasetyylikoliiniSynaptic TransmissionsolukalvotCell membranechemistry.chemical_compoundSCHIZOPHRENIAmolekyylidynamiikkamolecular dynamics (MD)neurotransmissionvälittäjäaineetChemistryLIPID-MEMBRANESGeneral NeurosciencePhosphatidylserineALZHEIMERS-DISEASEMembranemedicine.anatomical_structureHAMILTONIAN REPLICA EXCHANGElipids (amino acids peptides and proteins)dopamineIntracellularneurotransmittermonosialotetrahexosylganglioside (GM1)Synaptic cleftG(M1) GangliosideMolecular Dynamics SimulationNeurotransmission03 medical and health sciencesExtracellularmedicineAnimalsmonosialotetrahexosylgangliosidebinding free energyPhosphatidylglyceroldopamiiniBinding SitesCell Membranehistamiini3112 Neurosciencesta1182cholesterolBILAYERhistamineacetylcholinehermosolut030104 developmental biologyFORCE-FIELDBiophysicssynapsit
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Pistachio Consumption Prevents and Improves Lipid Dysmetabolism by Reducing the Lipid Metabolizing Gene Expression in Diet-Induced Obese Mice.

2018

Pistachios contain beneficial substances such as unsaturated fatty acids, phytosterols, and polyphenols. In the present study, we investigated if pistachio consumption is able to prevent or to revert hyperglycemia, dyslipidemia, hepatic steatosis, and adipose tissue morphological alterations caused by high fat diet (HFD) in the mouse. Moreover, the impact of pistachio intake on the mRNA expression of peroxisome proliferator-activated receptor &gamma

0301 basic medicineMaleAdipose tissueMice ObeseSettore BIO/09 - Fisiologiachemistry.chemical_compoundAdipocytelipid metabolizing gene expressionNutsHypertriglyceridemiaNutrition and Dieteticsbiologyfood and beveragesPhytosterolsFatty acid synthaseCholesterolAdipose TissueLiverPistacialipids (amino acids peptides and proteins)Sterol Regulatory Element Binding Protein 1lcsh:Nutrition. Foods and food supplyStearoyl-CoA Desaturasemedicine.medical_specialtyobesity-related dysfunctionslcsh:TX341-641pistachio consumptionDiet High-FatArticle03 medical and health sciencesInternal medicineobesity-related dysfunctionmedicineAnimalsObesityRNA MessengerDyslipidemias030109 nutrition & dieteticsFatty Acid Transport ProteinsPlant ExtractsHypertriglyceridemianutritional and metabolic diseasesPolyphenolsLipid metabolismmedicine.diseaseLipid MetabolismDietFatty LiverMice Inbred C57BLPPAR gammaEndocrinologychemistrybiology.proteinSteatosisFatty Acid SynthasesDiet-induced obeseFood ScienceNutrients
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Lipid Antigen Presentation by CD1b and CD1d in Lysosomal Storage Disease Patients

2019

The lysosome has a key role in the presentation of lipid antigens by CD1 molecules. While defects in lipid antigen presentation and in invariant Natural Killer T (iNKT) cell response were detected in several mouse models of lysosomal storage diseases (LSD), the impact of lysosomal engorgement in human lipid antigen presentation is poorly characterized. Here, we analyzed the capacity of monocyte-derived dendritic cells (Mo-DCs) from Fabry, Gaucher, Niemann Pick type C and Mucopolysaccharidosis type VI disease patients to present exogenous antigens to lipid-specific T cells. The CD1b- and CD1d-restricted presentation of lipid antigens by Mo-DCs revealed an ability of LSD patients to induce CD…

0301 basic medicineMaleAntigens CD1d / metabolismMucopolysaccharidosis type VIMonocytes / metabolismLysosomal Storage Diseases / diagnosisAntigens CD10302 clinical medicineAntigens CD1 / metabolismLysosomal storage diseaseImmunology and AllergyChildOriginal ResearchAged 80 and overAntigen PresentationbiologyKiller Cells Natural / metabolism*lipid antigen presentationAntigen Presentation / immunologyMiddle AgedNatural killer T cellLipidsnatural killer T cellsKiller Cells Naturalmedicine.anatomical_structureCD1DDendritic Cells / metabolismChild Preschool*dendritic cellsFemalelipids (amino acids peptides and proteins)*natural killer T cellsDisease SusceptibilitymonocytesAdultlcsh:Immunologic diseases. AllergyAdolescentT cellImmunologyCD1chemical and pharmacologic phenomenaCD1bLysosomal Storage Diseases / metabolismCD1dImmunophenotyping03 medical and health sciencesYoung AdultAntigenLysosomemedicineDendritic Cells / immunologyHumans*monocytesLymphocyte Countdendritic cellslysosomal storage diseasesLysosomal Storage Diseases / etiologyKiller Cells Natural / immunologyAgedbusiness.industry*CD1dInfantlipid antigen presentationmedicine.diseaseMonocytes / immunology*CD1b*lysosomal storage diseases030104 developmental biologyImmunologybiology.proteinAntigens CD1dbusinesslcsh:RC581-607Lipids / immunologyBiomarkers030215 immunology
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