2024
Lipid mediators in neutrophil biology: inflammation, resolution and beyond
Ghodsi A, Hidalgo A, Libreros S. Lipid mediators in neutrophil biology: inflammation, resolution and beyond. Current Opinion In Hematology 2024, 31: 175-192. PMID: 38727155, PMCID: PMC11301784, DOI: 10.1097/moh.0000000000000822.Peer-Reviewed Original ResearchConceptsG protein-coupled receptorsAcute inflammationLipid mediatorsResolution of acute inflammationChronic inflammatory disordersExcessive neutrophil infiltrationCell surface G protein-coupled receptorsEndogenous lipid mediatorsTissue repair mechanismsResolution of inflammationPro-resolving mediatorsNeutrophil infiltrationChronic inflammationIschemic eventsInflammatory disordersInflammatory insultInflammation sitesInflammationNeutrophil phagocytosisCardiovascular diseaseNeutrophil functionNeutrophilsTherapeutic agentsNeutrophil heterogeneityNeutrophil apoptosis
2023
Identification of a neutrophil-specific PIK3R1 mutation facilitates targeted treatment in a patient with Sweet syndrome
Bhattacharya S, Basu S, Sheng E, Murphy C, Wei J, Kersh A, Nelson C, Bryer J, Ashchyan H, Steele K, Forrestel A, Seykora J, Micheletti R, James W, Rosenbach M, Leung T. Identification of a neutrophil-specific PIK3R1 mutation facilitates targeted treatment in a patient with Sweet syndrome. Journal Of Clinical Investigation 2023, 133: e162137. PMID: 36355435, PMCID: PMC9797331, DOI: 10.1172/jci162137.Peer-Reviewed Original ResearchConceptsSteroid-sparing agentSweet's syndromeInflammatory diseasesCorticosteroid-related side effectsElevated IL-1Febrile neutrophilic dermatosisDramatic therapeutic responseReceptor 1 antagonistNeutrophil respiratory burstMultiorgan inflammatory diseasePersonalized medicine approachPI3K/AktSuccessful clinical interventionNeutrophilic dermatosisFrontline therapyRefractory casesNeutrophilic infiltrateBlood countIL-1βNeutrophil functionNeutrophil migrationTherapeutic responseLiver enzymesClinical challengeIL-1
2022
Neutrophilic Dermatoses: a Clinical Update
Weiss EH, Ko CJ, Leung TH, Micheletti RG, Mostaghimi A, Ramachandran SM, Rosenbach M, Nelson CA. Neutrophilic Dermatoses: a Clinical Update. Current Dermatology Reports 2022, 11: 89-102. PMID: 35310367, PMCID: PMC8924564, DOI: 10.1007/s13671-022-00355-8.Peer-Reviewed Original ResearchNeutrophilic eccrine hidradenitisSterile neutrophilic infiltratesAnti-inflammatory therapyAbnormal neutrophil functionRecent FindingsRecent studiesNeutrophilic dermatosisSweet's syndromeBehçet's syndromeClinicopathological featuresNeutrophilic infiltrateSignificant morbidityClinical updateNeutrophil functionComplex pathogenesisDrug reactionsExtracutaneous manifestationsInflammasome activationNeoplastic disordersGenetic predispositionMalignant transformationDermatosesSyndromePathogenesisTherapeutic frameworkDisorders
2021
Single-Cell Transcriptional Heterogeneity of Neutrophils During Acute Pulmonary Cryptococcus neoformans Infection
Deerhake ME, Reyes EY, Xu-Vanpala S, Shinohara ML. Single-Cell Transcriptional Heterogeneity of Neutrophils During Acute Pulmonary Cryptococcus neoformans Infection. Frontiers In Immunology 2021, 12: 670574. PMID: 33995406, PMCID: PMC8116703, DOI: 10.3389/fimmu.2021.670574.Peer-Reviewed Original ResearchConceptsPulmonary Cryptococcus neoformans infectionDistinct neutrophil subsetsCryptococcus neoformans infectionRole of neutrophilsLigand-receptor analysisCytokine gene expressionFirst-line defensePulmonary cryptococcosisNeoformans infectionDendritic cellsNeutrophil subsetsNeutrophil heterogeneityNeutrophil functionImmune cellsCell transcriptional heterogeneityAlveolar macrophagesNeutrophilsFungal infectionsCryptococcus neoformansInfectionSingle-cell transcriptional analysisGene expressionGenerate ROSOxidative stress signatureTranscriptional heterogeneity
2020
Aging exacerbates neutrophil pathogenicity in ischemic stroke
Roy-O'Reilly MA, Ahnstedt H, Spychala MS, Munshi Y, Aronowski J, Sansing LH, McCullough LD. Aging exacerbates neutrophil pathogenicity in ischemic stroke. Aging 2020, 12: 436-461. PMID: 31927534, PMCID: PMC6977697, DOI: 10.18632/aging.102632.Peer-Reviewed Original ResearchConceptsIschemic stroke patientsIschemic strokeNeutrophil-activating cytokineStroke patientsNeutrophil functionNeutrophil reactive oxygen speciesPoor post-stroke outcomesDepletion of neutrophilsPro-inflammatory functionsStrong risk factorExperimental mouse modelPost-stroke outcomesHigher stroke mortalityStroke outcomePoor outcomeFunctional outcomeStroke mortalityLong-term benefitsRisk factorsSpecific monoclonal antibodiesNeutrophil trafficTissue injuryYoung miceAged subjectsMouse model
2016
IL-17 Promotes Neutrophil-Mediated Immunity by Activating Microvascular Pericytes and Not Endothelium
Liu R, Lauridsen HM, Amezquita RA, Pierce RW, Jane-Wit D, Fang C, Pellowe AS, Kirkiles-Smith NC, Gonzalez AL, Pober JS. IL-17 Promotes Neutrophil-Mediated Immunity by Activating Microvascular Pericytes and Not Endothelium. The Journal Of Immunology 2016, 197: 2400-2408. PMID: 27534549, PMCID: PMC5010945, DOI: 10.4049/jimmunol.1600138.Peer-Reviewed Original ResearchMeSH KeywordsCaspase 9Cells, CulturedCulture MediaCytokinesEndothelium, VascularGranulocyte Colony-Stimulating FactorGranulocyte-Macrophage Colony-Stimulating FactorHumansInterleukin-17Neutrophil InfiltrationNeutrophilsPericytesReceptors, Interleukin-17Sequence Analysis, RNATumor Necrosis Factor-alphaVenulesConceptsIL-17Endothelial cellsIL-17RAIL-17RC subunitsCultured human endothelial cellsInflammatory gene expressionMicrovascular endothelial cellsNeutrophil-mediated immunityNeutrophil infiltrationNeutrophilic inflammationHuman endothelial cellsAcute inflammationIL-1βNeutrophil functionProinflammatory cytokinesIL-8Proinflammatory moleculesIL-1αIL-17RCIL-1Human pericytesG-CSFMicrovascular pericytesNeutrophil productionNeutrophil survival
2014
SRF is required for neutrophil migration in response to inflammation
Taylor A, Tang W, Bruscia EM, Zhang PX, Lin A, Gaines P, Wu D, Halene S. SRF is required for neutrophil migration in response to inflammation. Blood 2014, 123: 3027-3036. PMID: 24574460, PMCID: PMC4014845, DOI: 10.1182/blood-2013-06-507582.Peer-Reviewed Original ResearchMeSH KeywordsActin CytoskeletonActinsAnimalsBlotting, WesternCell AdhesionCell MovementChemokinesGene ExpressionInflammationIntegrinsMiceMice, KnockoutMice, TransgenicMicroscopy, ConfocalN-Formylmethionine Leucyl-PhenylalanineNeutrophilsPolymerizationReverse Transcriptase Polymerase Chain ReactionSerum Response FactorSignal TransductionConceptsKO neutrophilsNeutrophil functionNormal neutrophil numbersSerum response factorSites of inflammationRole of SRFLoss of SRFNeutrophil numbersNeutrophil migrationMalignant processNeutrophilsCytokine stimuliChemokine gradientsCell functionExpression levelsIntegrin expression levelsInflammationMicePrimary defenseMegakaryocyte maturationNormal cell functionVivoCellular adhesionMaster regulatorIntegrin activation
2013
A Network of Interactions Enables CCM3 and STK24 to Coordinate UNC13D-Driven Vesicle Exocytosis in Neutrophils
Zhang Y, Tang W, Zhang H, Niu X, Xu Y, Zhang J, Gao K, Pan W, Boggon TJ, Toomre D, Min W, Wu D. A Network of Interactions Enables CCM3 and STK24 to Coordinate UNC13D-Driven Vesicle Exocytosis in Neutrophils. Developmental Cell 2013, 27: 215-226. PMID: 24176643, PMCID: PMC3834565, DOI: 10.1016/j.devcel.2013.09.021.Peer-Reviewed Original ResearchConceptsNeutrophil degranulationAcute innate immune responseIschemia-reperfusion injuryInnate immune responseProtection of kidneyNeutrophil functionImmune responseInhibition of exocytosisTissue damageGranule poolGranule contentsDegranulationImportant regulatorImportant roleVesicle exocytosisExocytosisSTK24InjuryNeutrophilsKidneyUNC13D
2009
Inhibition of Neutrophil Function by Two Tick Salivary Proteins
Guo X, Booth CJ, Paley MA, Wang X, DePonte K, Fikrig E, Narasimhan S, Montgomery RR. Inhibition of Neutrophil Function by Two Tick Salivary Proteins. Infection And Immunity 2009, 77: 2320-2329. PMID: 19332533, PMCID: PMC2687334, DOI: 10.1128/iai.01507-08.Peer-Reviewed Original ResearchConceptsPolymorphonuclear leukocytesPMN functionNumber of PMNPMN integrinsPMN adherenceNeutrophil functionSpirochete burdenTick salivary proteinsTick salivaLyme diseaseTick attachmentSalivary glandsBorrelia burgdorferiTick feedingCausative agentReduced levelsInhibitory proteinSalivaBlood mealAntihemostatic activityInfectionInhibitionSalivary proteinsHematophagous arthropodsTick Ixodes scapularis
2008
Anaplasma phagocytophilum Increases Cathepsin L Activity, Thereby Globally Influencing Neutrophil Function
Thomas V, Samanta S, Fikrig E. Anaplasma phagocytophilum Increases Cathepsin L Activity, Thereby Globally Influencing Neutrophil Function. Infection And Immunity 2008, 76: 4905-4912. PMID: 18765732, PMCID: PMC2573316, DOI: 10.1128/iai.00851-08.Peer-Reviewed Original ResearchMeSH KeywordsAnaplasma phagocytophilumCathepsin LCathepsinsCysteine EndopeptidasesEhrlichiosisElectrophoretic Mobility Shift AssayGene Expression Regulation, BacterialHL-60 CellsHomeodomain ProteinsHumansImmunoblottingImmunoprecipitationNeutrophilsNuclear ProteinsRepressor ProteinsReverse Transcriptase Polymerase Chain ReactionTranscription FactorsConceptsA. phagocytophilum infectionPhagocytophilum infectionCathepsin L activityNeutrophil functionA. phagocytophilumL activityHuman neutrophil peptides 1Polymorphonuclear leukocyte functionNeutrophil peptide-1Human granulocytic anaplasmosisTherapeutic optionsNeutrophil defenseLeukocyte functionCathepsin LPeptide-1InfectionObligate intracellular pathogensMarked reductionGranulocytic anaplasmosisIntracellular pathogensCDP activityHost oxidative burstAnaplasma phagocytophilumPhagocytophilumOxidative burst
2006
Innate immunity defects in Hermansky-Pudlak type 2 syndrome
Fontana S, Parolini S, Vermi W, Booth S, Gallo F, Donini M, Benassi M, Gentili F, Ferrari D, Notarangelo L, Cavadini P, Marcenaro E, Dusi S, Cassatella M, Facchetti F, Griffiths G, Moretta A, Notarangelo L, Badolato R. Innate immunity defects in Hermansky-Pudlak type 2 syndrome. Blood 2006, 107: 4857-4864. PMID: 16507770, DOI: 10.1182/blood-2005-11-4398.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Protein Complex 3Adaptor Protein Complex beta SubunitsAdultAntigens, CDChildChild, PreschoolFemaleGene Expression RegulationHermanski-Pudlak SyndromeHumansImmunity, CellularImmunity, InnateImmunologic Deficiency SyndromesInfantKiller Cells, NaturalLeukocyte ElastaseMaleNeutrophilsPlatelet Membrane GlycoproteinsTetraspanin 30trans-Golgi NetworkConceptsAdaptor protein 3Hermansky-PudlakHermansky-Pudlak syndrome type 2Type 2 syndromeTrans-GolgiCargo proteinsBeta3A subunitAutosomal recessive diseaseDefects of innate immunityPlasma membraneNatural killerNK cellsInnate immunityInnate immune defectsAnalysis of neutrophilsRecessive diseaseIL-2-activated NK cellsPartial albinismLevels of perforinPathogenesis of immunodeficiencyUnstimulated NK cellsProtein 3Cytolitic activityImmune defectsNeutrophil function
2000
Sweet's syndrome and Pneumocystis carinii pneumonia: two sequelae of low‐dose cytosine arabinoside therapy in a patient with acute myeloid leukemia
Chowdhary V, Nityanand S, Prasad K, Pandey R, Dabadghao S. Sweet's syndrome and Pneumocystis carinii pneumonia: two sequelae of low‐dose cytosine arabinoside therapy in a patient with acute myeloid leukemia. European Journal Of Haematology 2000, 65: 72-73. PMID: 10914942, DOI: 10.1034/j.1600-0609.2000.9c177.x.Peer-Reviewed Original ResearchConceptsAcute myeloid leukemiaPneumocystis carinii pneumoniaMyeloid leukemiaCarinii pneumoniaLow‐dose cytosine arabinoside therapyAcute febrile neutrophilic dermatosisAttainment of remissionFebrile neutrophilic dermatosisLow-dose cytosineNeutrophilic dermatosisSweet's syndromeImmunosuppressive potentialNeutrophil functionLow doseLow dosesLeukemiaPneumoniaSyndromeDirect effectRemissionSequelaePatientsDermatosesTherapyDose
1999
Modulation of a calcium/calmodulin-dependent protein kinase cascade by retinoic acid during neutrophil maturation
Lawson N, Zain M, Zibello T, Picciotto M, Nairn A, Berliner N. Modulation of a calcium/calmodulin-dependent protein kinase cascade by retinoic acid during neutrophil maturation. Experimental Hematology 1999, 27: 1682-1690. PMID: 10560916, DOI: 10.1016/s0301-472x(99)00108-3.Peer-Reviewed Original ResearchConceptsKinase cascadeCaM kinase cascadeNeutrophil maturationRetinoic acidDependent protein kinase kinase alphaWestern analysisProtein kinase cascadeSpecific gene expressionImmediate early fashionNeutrophil-specific gene expressionTrans retinoic acidNeutrophil progenitor cellsRetinoic acid receptorsNeutrophil functionUninduced cellsGene expressionKinase alphaMyeloid cellsVitamin AAcid receptorsRetinoid signalingCell typesEffect of calciumProgenitor cellsProtein levels
1993
A 50-kDa integrin-associated protein is required for integrin-regulated calcium entry in endothelial cells.
Schwartz M, Brown E, Fazeli B. A 50-kDa integrin-associated protein is required for integrin-regulated calcium entry in endothelial cells. Journal Of Biological Chemistry 1993, 268: 19931-19934. PMID: 8376355, DOI: 10.1016/s0021-9258(20)80675-9.Peer-Reviewed Original ResearchConceptsIntegrin-associated proteinExtracellular matrix proteinsMatrix proteinsEndothelial cellsIAP functionTransmembrane domainTyrosine phosphorylationPrimary sequenceEndothelial cell adhesionCell adhesionMembrane channelsProteinAnti-integrin antibodiesCalcium entryCellsIntracellular pHIon transportInflux of Ca2Activation of neutrophilsActivationCalcium channelsCalcium influxPhosphorylationNeutrophil functionMonoclonal antibodies
1991
Modulation of Neonatal Neutrophil Function by Pentoxifylline
Krause P, Maderazo E, Contrino J, Eisenfeld L, Herson V, Greca N, Bannon P, Kreutzer D. Modulation of Neonatal Neutrophil Function by Pentoxifylline. Pediatric Research 1991, 29: 123-127. PMID: 2014147, DOI: 10.1203/00006450-199102000-00002.Peer-Reviewed Original ResearchConceptsPMN functionNitroblue tetrazolium reductionImpaired PMN functionsNeonatal neutrophil functionTetrazolium reductionTreatment of infectionsPolymorphonuclear leukocyte chemotaxisF-actin contentDose-dependent effectPotential clinical useCertain disease processesSimilar dose-dependent responseDose-dependent responseNeutrophil functionNewborn infantsPMN activityPMN deformabilityPMN chemotaxisDisease processPentoxifyllineLeukocyte chemotaxisMethylxanthine pentoxifyllinePhagocytic activityNeonatesClinical use
1989
Enhancement of neutrophil function for treatment of neonatal infections
KRAUSE P, HERSON V, EISENFELD L, JOHNSON G. Enhancement of neutrophil function for treatment of neonatal infections. The Pediatric Infectious Disease Journal 1989, 8: 382-389. PMID: 2664694, DOI: 10.1097/00006454-198906000-00011.Peer-Reviewed Original ResearchConceptsNewborn infantsRisk of morbidityFresh frozen plasmaMaximum therapeutic benefitHost defense mechanismsNeonatal infectionImportant therapyNeutrophil functionFrozen plasmaPMN functionTherapeutic benefitAdult PMNInfectionFurther studiesInfantsNew antibioticsDefense mechanismsTransfusionMorbidityNeonatesTherapyMortalityAdministrationImpairmentAntibodies
1988
Granulocyte-macrophage colony-stimulating factor enhances selective effector functions of tissue-derived macrophages.
Coleman D, Chodakewitz J, Bartiss A, Mellors J. Granulocyte-macrophage colony-stimulating factor enhances selective effector functions of tissue-derived macrophages. Blood 1988, 72: 573-8. PMID: 3042043, DOI: 10.1182/blood.v72.2.573.bloodjournal722573.Peer-Reviewed Original ResearchConceptsFc-dependent phagocytosisAnti-Toxoplasma activityGranulocyte-macrophage colony-stimulating factorGM-CSFColony-stimulating factorTissue-derived macrophagesRecombinant GM-CSFClass II major histocompatibility antigensMacrophage oxidative metabolismMajor histocompatibility antigensSite of exposureGM-CSF antibodyMurine recombinant GM-CSFThioglycollate-elicited cellsPhorbol myristate acetateNeutrophil functionHistocompatibility antigensEffector functionsVariety of cellsFunctional capacityMacrophage functionThioglycollate-elicited macrophagesResident macrophagesPeritoneal macrophagesStimulatory effectGranulocyte-Macrophage Colony-Stimulating Factor Enhances Selective Effector Functions of Tissue-Derived Macrophages
Coleman D, Chodakewitz J, Bartiss A, Mellors J. Granulocyte-Macrophage Colony-Stimulating Factor Enhances Selective Effector Functions of Tissue-Derived Macrophages. Blood 1988, 72: 573-578. DOI: 10.1182/blood.v72.2.573.573.Peer-Reviewed Original ResearchFc-dependent phagocytosisAnti-Toxoplasma activityGM-CSFTissue-derived macrophagesRecombinant GM-CSFClass II major histocompatibility antigensGranulocyte-macrophage colony-stimulating factorMacrophage oxidative metabolismMajor histocompatibility antigensSite of exposureGM-CSF antibodyColony-stimulating factorMurine recombinant GM-CSFThioglycollate-elicited cellsGranulocyte-macrophage colonyPhorbol myristate acetateNeutrophil functionHistocompatibility antigensEffector functionsVariety of cellsFunctional capacityMacrophage functionThioglycollate-elicited macrophagesResident macrophagesPeritoneal macrophages
1987
The Effect of Betamethasone on Neonatal Neutrophil Chemotaxis
Fuenfer M, Herson V, Raye J, Woronick C, Eisenfeld L, Ingardia C, Block C, Krause P. The Effect of Betamethasone on Neonatal Neutrophil Chemotaxis. Pediatric Research 1987, 22: 150-153. PMID: 3658539, DOI: 10.1203/00006450-198708000-00009.Peer-Reviewed Original ResearchConceptsEffect of betamethasoneBacterial infectionsNewborn infantsPMN functionMaternal glucocorticoid administrationNeonatal PMN functionFetal lung maturationMigration of PMNRandom migrationConcentrations of betamethasonePMN random migrationSignificant clinical importanceBetamethasone administrationGlucocorticoid administrationPregnant womenLung maturationNeutrophil functionStandard doseCord bloodNeutrophil chemotaxisAntiinflammatory agentsClinical importanceImportant causeImmune systemBetamethasoneHETEROGENEITY OF NEUTROPHIL (PMN) FUNCTION AND MONOCLONAL ANTIBODY (MAb) BINDING IN NEONATES AND ADULTS
Krause P, Bannon P, Eisenfeld L, Herson V, Kosciol K, Davidson K. HETEROGENEITY OF NEUTROPHIL (PMN) FUNCTION AND MONOCLONAL ANTIBODY (MAb) BINDING IN NEONATES AND ADULTS. Pediatric Research 1987, 21: 328-328. DOI: 10.1203/00006450-198704010-00964.Peer-Reviewed Original Research
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