Search results for "Interleukin 8"

showing 10 items of 57 documents

Budlein A from Viguiera robusta inhibits leukocyte-endothelial cell interactions, adhesion molecule expression and inflammatory mediators release

2009

Budlein A has been reported to exert some analgesic and anti-inflammatory properties. In this study, we have evaluated its effect on LPS-induced leukocyte recruitment in vivo and the mechanisms involved in its anti-inflammatory activity. In vivo, intravital videomicroscopy was used to determine the effects of budlein A on LPS-induced leukocyte-endothelial cell interactions in the murine cremasteric microcirculation. In vitro, the effects of budlein A on LPS-induced cytokine, chemokine and nitrites release, T-cell proliferative response as well as cell adhesion molecule expression (CAM) were evaluated. In vivo, intraperitoneal administration of budlein A (2.6 mM/kg) caused a significant redu…

LipopolysaccharidesMaleChemokineT-Lymphocytesmedicine.medical_treatmentPharmaceutical ScienceLeukocyte RollingCell CommunicationAsteraceaeNitric OxideDexamethasoneCell LineLactonesMiceIn vivoDrug DiscoverymedicineAnimalsHumansLeukocyte RollingInterleukin 8NitritesCell ProliferationPharmacologyMice Inbred BALB CbiologyPlant ExtractsCell adhesion moleculeMacrophagesMicrocirculationMonocyteEndothelial CellsCell biologyMice Inbred C57BLEndothelial stem cellmedicine.anatomical_structureCytokineComplementary and alternative medicinebiology.proteinMolecular MedicineChemokinesCell Adhesion MoleculesSesquiterpenesImmunosuppressive AgentsPhytomedicine
researchProduct

A role for Toll-like receptor mediated signals in neutrophils in the pathogenesis of the anti-phospholipid syndrome.

2012

The anti-phospholipid syndrome (APS) is characterized by recurrent thrombosis and occurrence of anti-phospholipid antibodies (aPL). aPL are necessary, but not sufficient for the clinical manifestations of APS. Growing evidence suggests a role of innate immune cells, in particular polymorphonuclear neutrophils (PMN) and Toll-like receptors (TLR) to be additionally involved. aPL activate endothelial cells and monocytes through a TLR4-dependent signalling pathway. Whether this is also relevant for PMN in a similar way is currently not known. To address this issue, we used purified PMN from healthy donors and stimulated them in the presence or absence of human monoclonal aPL and the TLR4 agonis…

LipopolysaccharidesNeutrophilsImmunology610 MedizinImmunoglobulinslcsh:MedicineInflammationApoptosisImmunopathologyBiologyNeutrophil ActivationAutoimmune DiseasesPhagocytosisimmune system diseases610 Medical sciencesmedicineHumansInterleukin 8L-SelectinReceptorlcsh:ScienceBiologyImmune ResponseneoplasmsRespiratory BurstInflammationToll-like receptorMultidisciplinaryInnate immune systemCD11b AntigenCoagulation DisordersEffectorInterleukin-8lcsh:RImmunityHematologyAntiphospholipid SyndromeFlow CytometryInnate ImmunityRespiratory burstToll-Like Receptor 4ImmunologyTLR4MedicineClinical Immunologylcsh:Qmedicine.symptomResearch ArticleSignal TransductionPLoS ONE
researchProduct

Sphingosine-1-phosphate increases human alveolar epithelial IL-8 secretion, proliferation and neutrophil chemotaxis

2009

Sphingosine-1-phosphate (S1P) has been presented recently as a pro-inflammatory agent in the airway epithelium since S1P levels are increased in bronchoalveolar lavage fluid of human asthmatics. However, the effects of S1P over the alveolar epithelium and neutrophil interactions are poorly understood. Here, we show that S1P increased interleukin 8 (IL-8) gene expression and protein secretion and proliferation in alveolar epithelial cells A549 at physiological concentrations (1 microM). At the same time, S1P increased intracellular Ca2+ concentration (potency 17.91 microM, measured by epifluorescence microscopy), phospholipase D (PLD) activity (measured by chemiluminiscence method) and extra…

LuminescenceNeutrophilsIntercellular Adhesion Molecule-1Gene ExpressionBiologyPertussis toxinReceptors G-Protein-Coupled1-ButanolSphingosineCell Line TumorPhospholipase DHumansInterleukin 8PhosphorylationExtracellular Signal-Regulated MAP KinasesEgtazic AcidCell ProliferationFlavonoidsPharmacologyA549 cellCell adhesion moleculeInterleukin-8Epithelial CellsChemotaxisIntercellular Adhesion Molecule-1Intercellular adhesion moleculeMolecular biologyPulmonary AlveoliChemotaxis LeukocytePertussis ToxinBiochemistryRespiratory epitheliumCalciumlipids (amino acids peptides and proteins)LysophospholipidsEuropean Journal of Pharmacology
researchProduct

Role of meprins to protect ileal mucosa of Crohn's disease patients from colonization by adherent-invasive E. coli

2011

Ileal lesions in Crohn's disease (CD) patients are colonized by pathogenic adherent-invasive Escherichia coli (AIEC) able to adhere to and invade intestinal epithelial cells (IEC), and to survive within macrophages. The interaction of AIEC with IEC depends on bacterial factors mainly type 1 pili, flagella, and outer membrane proteins. In humans, proteases can act as host defence mechanisms to counteract bacterial colonization. The protease meprin, composed of multimeric complexes of the two subunits alpha and beta, is abundantly expressed in IECs. Decreased levels of this protease correlate with the severity of the inflammation in patients with inflammatory bowel disease. The aim of the pre…

MaleBacterial Diseasesmedicine.medical_treatmentACTIVATION MECHANISMBiochemistryBacterial AdhesionPilusMice0302 clinical medicineCrohn DiseaseIntestinal mucosaMolecular Cell BiologyGastrointestinal InfectionsIntestinal MucosaAged 80 and over0303 health sciencesMultidisciplinaryQRMetalloendopeptidasesMiddle AgedEnzymesBacterial Pathogens3. Good healthHost-Pathogen InteractionInfectious DiseasesCytokineESCHERICHIA-COLI030220 oncology & carcinogenesisAlimentation et NutritionMedicineFemaleINFLAMMATORY-BOWEL-DISEASE;INTESTINAL EPITHELIAL-CELLS;URINARY-TRACT-INFECTIONS;ESCHERICHIA-COLI;ALPHA-SUBUNIT;STRAIN LF82;METALLOPROTEASE MEPRIN;ACTIVATION MECHANISM;BETA-SUBUNIT;TYPE-1 PILICellular Typesmedicine.symptomBacterial outer membraneALPHA-SUBUNITResearch ArticleAdultProteasesScienceMédecine humaine et pathologieInflammationGastroenterology and HepatologyBiologyMETALLOPROTEASE MEPRINMicrobiologyMicrobiologyURINARY-TRACT-INFECTIONS03 medical and health sciencesTYPE-1 PILIEscherichia colimedicineAnimalsHumansFood and NutritionSecretionInterleukin 8BETA-SUBUNITBiologyAged030304 developmental biologySTRAIN LF82Interleukin-8Inflammatory Bowel DiseaseEpithelial Cellsdigestive system diseasesMice Inbred C57BLHuman health and pathologyINTESTINAL EPITHELIAL-CELLS[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyINFLAMMATORY-BOWEL-DISEASE
researchProduct

Exosome-mediated crosstalk between chronic myelogenous leukemia cells and human bone marrow stromal cells triggers an Interleukin 8-dependent surviva…

2014

Chronic myelogenous leukemia (CML) is a myeloproliferative disorder characterized by the Bcr-Abl oncoprotein with constitutive tyrosine kinase activity. Exosomes are nanovesicles released by cancer cells that are involved in cell-to-cell communication thus potentially affecting cancer progression. It is well known that bone marrow stromal microenvironment contributes to disease progression through the establishment of a bi-directional crosstalk with cancer cells. Our hypothesis is that exosomes could have a functional role in this crosstalk. Interleukin-8 (IL 8) is a proinflammatory chemokine that activates multiple signalling pathways downstream of two receptors (CXCR1 and CXCR2). We demon…

MaleCancer ResearchChemokineStromal cellCell SurvivalMice SCIDExosomesChronic myelogenous leukemia Bone marrow stromal cells Tumour microenvironment Exosomes Interleukin 8ExosomeMiceCell MovementMice Inbred NODSettore BIO/13 - Biologia ApplicataCell Line TumorLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesParacrine CommunicationCell AdhesionTumor MicroenvironmentmedicineAnimalsHumansCXC chemokine receptorsStem Cell NichebiologyInterleukin-8Mesenchymal Stem Cellsmedicine.diseaseUp-RegulationLeukemiaPhenotypemedicine.anatomical_structureOncologyCancer cellImmunologyCancer researchbiology.proteinHeterograftsBone marrowSignal TransductionChronic myelogenous leukemiaCancer Letters
researchProduct

Control of Cell Migration and Inflammatory Mediators Production by CORM-2 in Osteoarthritic Synoviocytes

2011

Background Osteoarthritis (OA) is the most widespread degenerative joint disease. Inflamed synovial cells contribute to the release of inflammatory and catabolic mediators during OA leading to destruction of articular tissues. We have shown previously that CO-releasing molecules exert anti-inflammatory effects in animal models and OA chondrocytes. We have studied the ability of CORM-2 to modify the migration of human OA synoviocytes and the production of chemokines and other mediators sustaining inflammatory and catabolic processes in the OA joint. Methodology/Principal Findings OA synoviocytes were stimulated with interleukin(IL)-1β in the absence or presence of CORM-2. Migration assay was…

MaleChemokineAnatomy and PhysiologyInterleukin-1betalcsh:MedicineGene ExpressionMatrix metalloproteinaseBiochemistryCell MovementDrug Discoverylcsh:ScienceMusculoskeletal SystemCells CulturedChemokine CCL2MultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionSynovial MembraneNF-kappa BInterleukinCell migrationmedicine.anatomical_structureMedicineFemaleMatrix Metalloproteinase 3Inflammation MediatorsMatrix Metalloproteinase 1Mitogen-Activated Protein KinasesResearch ArticleCell PhysiologyBlotting WesternRheumatologySynovitisOsteoarthritisOrganometallic CompoundsmedicineHumansInterleukin 8BiologyAgedCell ProliferationChemokine CCL20lcsh:RInterleukin-8medicine.diseaseTranscription Factor AP-1CCL20Oxidative StressSmall MoleculesImmunologyCancer researchbiology.proteinlcsh:QSynovial membraneHeme Oxygenase-1PLoS ONE
researchProduct

Analysis of immunosuppressive factors produced by tumorspheres in NSCLC: Prognostic value of galectin-3 in adenocarcinoma

2019

Abstract Background Cancer stem cells (CSCs) are targets poorly recognized by the immune surveillance system given that they induce an immunosuppressive microenvironment. The aim of this work is to study the interactions between CSCs and the immune microenvironment in NSCLC. Methods Tumor cells from 8 resected NSCLC patients and 12 cell lines were established as tumorspheres enriched in CSCs and as monolayers. The gene expression of IL-4, IL-10, IL6, IL8 and LGALS-3 was analyzed by RTqPCR. Results were validated at a protein level by a sensitivity bead-based multiplex immunoassay using the Millipore kit for Luminex 100/200. The prognostic value of these factors in silico was determined in a…

Oncologymedicine.medical_specialtyLungbusiness.industryProportional hazards modelHematologymedicine.diseasemedicine.anatomical_structureOncologyGalectin-3Cancer stem cellInternal medicineGene expressionmedicineAdenocarcinomaInterleukin 8businessSurvival analysisAnnals of Oncology
researchProduct

Phospho-p38 MAPK expression in COPD patients and asthmatics and in challenged bronchial epithelium

2015

<b><i>Background:</i></b> The role of mitogen-activated protein kinases (MAPK) in regulating the inflammatory response in the airways of patients with chronic obstructive pulmonary disease (COPD) and asthmatic patients is unclear. <b><i>Objectives:</i></b> To investigate the expression of activated MAPK in lungs of COPD patients and in bronchial biopsies of asthmatic patients and to study MAPK expression in bronchial epithelial cells in response to oxidative and inflammatory stimuli. <b><i>Methods:</i></b> Immunohistochemical expression of phospho (p)-p38 MAPK, p-JNK1 and p-ERK1/2 was measured in bronchial mucosa in pat…

P38 MAPKMaleMAPK/ERK pathwayAsthma phenotypeSMOKERespiratory SystemMitogen-activated protein kinases; p65; Pathology of chronic obstructive pulmonary disease; Chronic obstructive pulmonary disease phenotypes; Asthma phenotypesPathology of chronic obstructive pulmonary diseasep38 Mitogen-Activated Protein KinasesChronic obstructive pulmonary disease phenotypePulmonary Disease Chronic ObstructiveOXIDATIVE STRESSMACROPHAGESRespiratory systemMitogen-activated protein kinasesChronic obstructive pulmonary disease phenotypesMitogen-activated protein kinases; p65; pathology of chronic obstructive pulmonary disease phenotypes; asthma phenotypesCOPDp65KinaseAsthma phenotypes; Chronic obstructive pulmonary disease phenotypes; Mitogen-activated protein kinases; p65; Pathology of chronic obstructive pulmonary disease; Pulmonary and Respiratory MedicineACTIVATED PROTEIN-KINASEInterleukinMiddle AgedImmunohistochemistrypathology of chronic obstructive pulmonary disease phenotypesAsthma phenotypesFemaleLife Sciences & BiomedicinePulmonary and Respiratory Medicinep38 mitogen-activated protein kinasesBlotting WesternINHIBITIONSocio-culturaleBronchiRespiratory MucosaOBSTRUCTIVE PULMONARY-DISEASE1102 Cardiovascular Medicine And HaematologyCell LinemedicineHumansLymphocyte CountInterleukin 8AgedAsthmaScience & Technologybusiness.industryInterleukin-8Transcription Factor RelAPATHWAYSMitogen-activated protein kinasemedicine.diseaseAsthmarespiratory tract diseasesSEVERITYCase-Control StudiesCELLSImmunologybusiness
researchProduct

Effects of nano-scaled particles on endothelial cell function in vitro: studies on viability, proliferation and inflammation.

2004

Recent studies give support for a connection between the presence of inorganic particles (of microm and nm size) in different organs and tissues and the development of inflammatory foci, called granulomas. As the potential source of particles (e.g. porcelain dental bridges) and the location of particle detection were topographically far apart, a distribution via the blood stream appears highly probable. Thus, endothelial cells, which line the inner surface of blood vessels, would come into direct contact with these particles, making particle-endothelial interactions potentially pathogenically relevant. The objective of this study was to evaluate the effects that five different nano-scaled p…

Pathologymedicine.medical_specialtyMaterials scienceEffectsCell divisionCell Survivalnano-scaledproliferationCellBiomedical EngineeringBiophysicsBiocompatible MaterialsBioengineeringInflammationBiomaterialsNickelIn vivoMaterials TestingendothelialmedicineHumansInterleukin 8Particle SizePolyvinyl ChlorideCells CulturedTitaniumparticlesfunctionNanotubesForeign-Body ReactionviabilityInterleukin-8Endothelial Cellsin vitroCobaltcellSilicon DioxideEndothelial stem cellKi-67 Antigenmedicine.anatomical_structureinflammationBiophysicsParticle sizemedicine.symptomEffects; nano-scaled; particles; endothelial; cell; function; in vitro; viability; proliferation; inflammationCell DivisionBlood vessel
researchProduct

Spatial and temporal heterogeneity of ventilator-associated lung injury after surfactant depletion.

2008

Volutrauma and atelectrauma have been proposed as mechanisms of ventilator-associated lung injury, but few studies have compared their relative importance in mediating lung injury. The objective of our study was to compare the injury produced by stretch (volutrauma) vs. cyclical recruitment (atelectrauma) after surfactant depletion. In saline-lavaged rabbits, we used high tidal volume, low respiratory rate, and low positive end-expiratory pressure to produce stretch injury in nondependent lung regions and cyclical recruitment in dependent lung regions. Tidal changes in shunt fraction were assessed by measuring arterial Po2 oscillations. After ventilating for times ranging from 0 to 6 h, lu…

Pathologymedicine.medical_specialtyVentilator-associated lung injuryPhysiologyNitric Oxide Synthase Type IIInflammationEnzyme-Linked Immunosorbent AssayPulmonary EdemaRespiratory physiologyLung injuryPhysiology (medical)medicineAnimalsInterleukin 8LungChemokine CCL2PeroxidaseLungVentilators Mechanicalbusiness.industryRespiratory diseaseInterleukin-8Pulmonary SurfactantsLung Injuryrespiratory systemmedicine.diseasePulmonary edemarespiratory tract diseasesOxygenmedicine.anatomical_structureNeutrophil InfiltrationCalibrationRespiratory MechanicsCytokinesFluid TherapyFemaleRabbitsmedicine.symptomBlood Gas AnalysisChemokinesbusinessJournal of applied physiology (Bethesda, Md. : 1985)
researchProduct