Search results for "Cell Degranulation"

showing 10 items of 26 documents

Mast cells promote homeostasis by limiting endothelin-1-induced toxicity

2004

Endothelin-1 (ET-1) is a 21-amino-acid peptide, derived from vascular endothelial cells, with potent vasoconstrictor activity. ET-1 has been implicated in diverse physiological or pathological processes, including the vascular changes associated with sepsis. However, the factors that regulate ET-1-associated toxicity during bacterial infections, or in other settings, are not fully understood. Both the pathology associated with certain allergic and autoimmune disorders, and optimal host defence against bacterial and parasitic infections are mediated by mast cells. In vitro, mast cells can produce ET-1 (ref. 11), undergo ET-1-dependent and endothelin-A receptor (ET(A))-dependent activation, a…

DiarrheaProteasesDrug-Related Side Effects and Adverse ReactionsCell SurvivalPeritonitisBiologyPeptides CyclicCell DegranulationBody TemperatureMiceChymasesIn vivomedicineAnimalsHomeostasisMast CellsReceptorEgtazic AcidMice KnockoutMultidisciplinaryEndothelin-1Stem CellsBody WeightSerine EndopeptidasesEndogenous mediatorMast cellEndothelin 1In vitroCell biologyMice Inbred C57BLSurvival RateProto-Oncogene Proteins c-kitmedicine.anatomical_structureMutationImmunologyFemaleOligopeptidesInjections IntraperitonealHomeostasisNature
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Inflammatory Murine Skin Responses to UV-B Light Are Partially Dependent on Endothelin-1 and Mast Cells

2006

Endothelin (ET-1) has been shown to crucially contribute to UV-induced skin responses such as tanning. To test whether ET-1 is also involved in early cutaneous reactions to UV, we assessed ET-1 skin levels in UV-irradiated mice. In correlation with the levels of UV-induced skin inflammation, ET-1 concentrations increased substantially and continually. Moreover, blocking of ET-1 receptors (ET A ) resulted in significantly decreased cutaneous inflammation following UV irradiation. When we assessed skin responses to ET-1 injections, we observed prominent mast cell degranulation and mast cell-dependent inflammation. Since mast cells also critically contributed to UV-induced inflammation, we det…

Endothelin A Receptor AntagonistsUltraviolet RaysCell DegranulationRatónDermatitisMice TransgenicInflammationBiologyPharmacologyCell DegranulationPathology and Forensic MedicineMicemedicineAnimalsMast CellsReceptorInflammationEndothelin-1integumentary systemDegranulationDose-Response Relationship RadiationReceptor Endothelin AMast cellEndothelin 1medicine.anatomical_structureImmunologymedicine.symptomEndothelin receptorRegular ArticlesThe American Journal of Pathology
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Classical and alternative pathways of mast cell activation.

2002

It has long since been recognized that mast cells are critical effectors of anaphylactic reactions, and the existence of these potentially hazardous cells has solely been justified due to their beneficial role in some infections with extracellular parasites. A novel understanding of mast cells as sentinels of the immune system has been made possible by taking advantage of mast cell-deficient mice in order to study the roles of mast cells in vivo and by detailed analyses of mast cell activation in vitro. Collectively, these experiments have revealed a variety of IgE-independent stimuli, which lead to the activation of mast cells as crucial initiators of an inflammatory response. Besides thei…

InflammationCell typeAdenosinePolymers and PlasticsEndothelin-1EffectorReceptors IgEBiologyInfectionsNeurosecretory SystemsIn vitroCell DegranulationCell biologyDisease Models AnimalImmune systemGene Expression RegulationIn vivoImmune SystemImmunoglobulin GExtracellularAnimalsMast CellsReceptorFunction (biology)General Environmental ScienceCritical reviews in immunology
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Synthesis and evaluation of 2-tosylamino and 2-tosyliminopyrimidine derivatives as inhibitors of some leukocyte functions

2003

Abstract We have studied the potential anti-inflammatory effects of 20 2-tosylamino and 2-tosyliminopyrimidine new derivatives in human neutrophils. We have evaluated their interference with some leukocyte functions and 5-lipoxygenase activity. All the compounds reduced neutrophil degranulation process at concentrations in the μM range. Besides, compounds with a phenolic substitution inhibited leukotriene B 4 biosynthesis in neutrophils and decreased the cell-free 5-lipoxygenase activity. This study demonstrates that 2-tosylamino and 2-tosyliminopyrimidine derivatives can reduce the activation of neutrophil cells which may have relevance for the modulation of the inflammatory response.

Magnetic Resonance SpectroscopyNeutrophilsLeukotriene B4Inflammatory responseCell SeparationIn Vitro TechniquesLeukotriene B4Cell DegranulationTosyl Compounds2-tosyliminopyrimidinechemistry.chemical_compoundLipoxygenaseBiosynthesisDrug DiscoveryLeukocytesHumansLipoxygenase InhibitorsPharmacologychemistry.chemical_classificationArachidonate 5-LipoxygenasebiologyChemistryOrganic ChemistryElastaseGeneral MedicineIn vitroPyrimidinesEnzymeBiochemistryEnzyme inhibitorArachidonate 5-lipoxygenaseLeukotriene Bbiology.proteinNeutrophil degranulationIndicators and ReagentsLeukocyte ElastaseEuropean Journal of Medicinal Chemistry
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Mast cell targeting hampers prostate adenocarcinoma development but promotes the occurrence of highly malignant neuroendocrine cancers

2011

Abstract Mast cells (MC) are c-Kit–expressing cells, best known for their primary involvement in allergic reactions, but recently reappraised as important players in either cancer promotion or inhibition. Here, we assessed the role of MCs in prostate tumor development. In prostate tumors from both tumor-prone transgenic adenocarcinoma of the mouse prostate (TRAMP) mice and human patients, MCs are specifically enriched and degranulated in areas of well-differentiated (WD) adenocarcinoma but not around poorly differentiated (PD) foci that coexist in the same tumors. We derived novel TRAMP tumor cell lines, representative of WD and PD variants, and through pharmacologic stabilization or geneti…

MaleOncologyCancer Researchmedicine.medical_specialtyEpithelial-Mesenchymal TransitionMice TransgenicAdenocarcinomaBiologymedicine.disease_causeCell DegranulationMiceProstate cancerProstateCell Line TumorInternal medicineTumor MicroenvironmentmedicineMast CellAnimalsHumansMast CellsReceptors Tumor Necrosis Factor Member 25Tumor microenvironmentAdenocarcinoma; Animals; Carcinoma Neuroendocrine; Cell Degranulation; Cell Line Tumor; Disease Progression; Epithelial-Mesenchymal Transition; Humans; Male; Mast Cells; Matrix Metalloproteinase 9; Mice; Mice Inbred C57BL; Mice Transgenic; Prostatic Neoplasms; Proto-Oncogene Proteins c-kit; Receptors Tumor Necrosis Factor Member 25; Tumor Microenvironment; Cancer Research; OncologyAnimalProstatic NeoplasmsCancermedicine.diseasehumanitiesCarcinoma NeuroendocrineMice Inbred C57BLProto-Oncogene Proteins c-kitmedicine.anatomical_structureMatrix Metalloproteinase 9OncologyTumor progressionProstatic NeoplasmDisease ProgressionAdenocarcinomaCarcinogenesisHumanTramp
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Characterization of neutrophil subsets in healthy human pregnancies

2014

We have previously shown that in successful pregnancies increased arginase activity is a mechanism that contributes to the suppression of the maternal immune system. We identified the main type of arginase-expressing cells as a population of activated low-density granulocytes (LDGs) in peripheral blood mononuclear cells and in term placentae. In the present study, we analyzed the phenotype of LDGs and compared it to the phenotype of normal density granulocytes (NDGs) in maternal peripheral blood, placental biopsies and cord blood. Our data reveal that only LDGs but no NDGs could be detected in placental biopsies. Phenotypically, NDGs and LDGs from both maternal and cord blood expressed diff…

NeutrophilsPlacentaEnzyme Metabolismlcsh:MedicineGene ExpressionBiochemistryCell DegranulationNeutrophil ActivationImmune toleranceLeukocyte Count0302 clinical medicineImmunophenotypingPregnancyMolecular Cell BiologySUPPRESSOR-CELLSlcsh:Science0303 health scienceseducation.field_of_studyMultidisciplinaryL-ARGININEObstetrics and GynecologyFetal BloodInnate Immunity3. Good healthEnzymesmedicine.anatomical_structurePhenotypeARGINASE ACTIVITYCord bloodMedicineScience & Technology - Other TopicsFemaleBiological MarkersTHERAPEUTIC PERSPECTIVESResearch ArticleEXPRESSIONAdultCordGeneral Science & TechnologyImmune CellsPopulationImmunologyBiologyMETABOLISMGRANULOCYTESGPI-Linked ProteinsPeripheral blood mononuclear cellMECHANISMSImmunophenotyping03 medical and health sciencesImmune systemAntigens CDPlacentaMD MultidisciplinarymedicineImmune ToleranceHumansCell LineageeducationBiology030304 developmental biologyScience & TechnologyArginaseMULTIDISCIPLINARY SCIENCESlcsh:RImmunityOXIDANT RELEASEImmunologyWomen's Healthlcsh:QClinical ImmunologyIMMUNE-SYSTEMCell Adhesion MoleculesCytometryBiomarkers030215 immunology
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Direct evidence that FK506 inhibition of FcεRI-mediated exocytosis from RBL mast cells involves calcineurin

1998

eRI-mediated exocytosis of preformed mediators from mast cells and basophils (e.g. histamine, serotonin, beta-hexosaminidase) is sensitive to the immunosuppressants cyclosporin A and FK506 (IC 50 200 and 4 n M , respectively) but not rapamycin. The mechanism of inhibition does not appear to involve tyrosine phosphorylation, hydrolysis of inositol phosphates or calcium flux. Here we report experiments using a molecular approach to assess the role of calcineurin, a serine/threonine phosphatase thought to be the primary pharmacological target of these drugs. Calcineurin’s activity requires association of its catalytic (A) subunit with an intrinsic regulatory (B) subunit. We hypothesized that c…

Protein subunitDermatologyBiologyTransfectionSensitivity and SpecificityCell DegranulationExocytosisTacrolimusExocytosischemistry.chemical_compoundCyclosporin aCalcium fluxTumor Cells CulturedmedicineAnimalsMast CellsDose-Response Relationship DrugReceptors IgECalcineurinTyrosine phosphorylationGeneral MedicineMast cellRatsCell biologyCalcineurinElectroporationmedicine.anatomical_structureLeukemia Basophilic AcutechemistryBiochemistryImmunosuppressive AgentsHistamineArchives of Dermatological Research
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Technical Advance:Soluble OX40 molecule mimics regulatory T cell modulatory activity on Fc{varepsilon}RI-dependent mast cell degranulation.

2011

Tregs play a central role in modulating FcεRI-dependent MC effector functions in the course of the allergic response. Cellular interaction depends on the constitutive expression of OX40 on Tregs and the OX40L counterpart on MCs. Study of OX40L signaling on MCs is hampered by the need of a highly purified molecule, which triggers OX40L specifically. We now report that sOX40 mimics the physiological activity of Treg interaction by binding to activated MCs. When treated with sOX40, activated MCs showed decreased degranulation and Ca++ influx, whereas PLC-γ2 phosphorylation remained unaffected. Once injected into experimental animals, sOX40 not only located within the endothelium but also in pa…

T cell modulatory activitySoluble OX40Soluble OX40; T cell modulatory activity; Fc{varepsilon}RI-dependent mast cell degranulationFc{varepsilon}RI-dependent mast cell degranulation
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CD4+CD25+ regulatory T cells suppress mast cell degranulation and allergic responses through OX40-OX40L interaction.

2008

T regulatory (Treg) cells play a role in the suppression of immune responses, thus serving to induce tolerance and control autoimmunity. Here, we explored whether Treg cells influence the immediate hypersensitivity response of mast cells (MCs). Treg cells directly inhibited the FcεRI-dependent MC degranulation through cell-cell contact involving OX40-OX40L interactions between Treg cells and MCs, respectively. When activated in the presence of Treg cells, MCs showed increased cyclic adenosine monophosphate (cAMP) concentrations and reduced Ca2+ influx, independently of phospholipase C (PLC)-γ2 or Ca2+ release from intracellular stores. Antagonism of cAMP in MCs reversed the inhibitory effec…

T-LymphocytesCELLIMMUNO; Animals; Calcium; Cell Line Tumor; Gene Knockdown Techniques; Histamine Release; Humans; Hypersensitivity; Mast Cells; Membrane Glycoproteins; Mice; Mice Inbred BALB C; Mice Inbred C57BL; Phospholipase C gamma; Receptors OX40; T-Lymphocytes Regulatory; Tumor Necrosis Factors; Cell Degranulation; Immunology and Allergy; Infectious Diseases; ImmunologyInbred C57BLmedicine.disease_causeHistamine ReleaseT-Lymphocytes RegulatoryCell DegranulationAutoimmunityMicechemistry.chemical_compoundReceptorsImmunology and AllergyOX40Mast CellsInbred BALB CMice Inbred BALB CTumorMembrane GlycoproteinsDegranulationhemic and immune systemsRegulatoryhumanitiesCell biologyTregInfectious DiseasesGene Knockdown TechniquesTumor Necrosis FactorsMembrane GlycoproteinMast cell; Treg; OX40-OX40L interactionIntracellularHumanCell DegranulationImmunologyInfectious Diseasechemical and pharmacologic phenomenaBiologybehavioral disciplines and activitiesArticleCell LineMast cellImmune systemCell Line TumorHypersensitivitymedicineAnimalsHumansCyclic adenosine monophosphatePhospholipase CAnimalPhospholipase C gammaReceptors OX40Mice Inbred C57BLchemistryCELLIMMUNOCell cultureGene Knockdown TechniqueImmunologyOX40-OX40L interactionCalciumTumor Necrosis Factor
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The aryl hydrocarbon receptor modulates acute and late mast cell responses.

2012

Abstract The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activity is modulated by xenobiotics as well as physiological ligands. These compounds may modulate inflammatory responses and contribute to the rising prevalence of allergic diseases observed in industrialized countries. Mast cells (MCs), located within tissues at the boundary of the external environment, represent a potential target of AhR ligands. In this study, we report that murine and human MCs constitutively express AhR, and its activation by the high-affinity ligand 6-formylindolo[3,2-b]carbazole (FICZ) determines a boost in degranulation. On the contrary, repeated exposure to FICZ inhibits…

Time FactorsInbred C57BLLigandsCell DegranulationPathogenesischemistry.chemical_compoundMiceAnaphylaxiReceptorsMast CellImmunology and AllergyMast CellsReceptorMice KnockoutbiologyInterleukin-17DegranulationMast cellUp-RegulationImmunology Mast Cell Aryl Receptormedicine.anatomical_structureAryl HydrocarbonBone Marrow Celldeficiency/metabolism/physiologyIgEmedicine.symptomimmunology/metabolism/pathologyHistamineHumanReceptorTime FactorKnockoutImmunologyDown-RegulationLigandInflammationBone Marrow CellsSettore MED/08 - Anatomia PatologicaCell LinebiosynthesiAnaphylaxis; immunology/metabolism/pathology Animals Bone Marrow Cells; immunology/metabolism/pathology Cell Degranulation; genetics/immunology Cell Line Down-Regulation; genetics/immunology Humans Interleukin-17; biosynthesis Interleukin-6; biosynthesis Ligands Mast Cells; immunology/metabolism/pathology Mice Mice; Inbred C57BL Mice; Knockout Receptors; Aryl Hydrocarbon; deficiency/metabolism/physiology Receptors; IgE; physiology Time Factors Up-Regulation; genetics/immunologymedicineAnimalsHumansTranscription factorAnaphylaxisAnimalInterleukin-6Receptors IgEAryl hydrocarbon receptorgenetics/immunologyMice Inbred C57BLMAST CELL; ARYL HYDROCARBON RECEPTORchemistryReceptors Aryl HydrocarbonImmunologyphysiologybiology.proteinbiosynthesisJournal of immunology (Baltimore, Md. : 1950)
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