2024
Ezrin drives adaptation of monocytes to the inflamed lung microenvironment
Gudneppanavar R, Di Pietro C, H Öz H, Zhang P, Cheng E, Huang P, Tebaldi T, Biancon G, Halene S, Hoppe A, Kim C, Gonzalez A, Krause D, Egan M, Gupta N, Murray T, Bruscia E. Ezrin drives adaptation of monocytes to the inflamed lung microenvironment. Cell Death & Disease 2024, 15: 864. PMID: 39613751, PMCID: PMC11607083, DOI: 10.1038/s41419-024-07255-8.Peer-Reviewed Original ResearchConceptsActivation of focal adhesion kinaseExtracellular matrixActin-binding proteinsFocal adhesion kinaseLung extracellular matrixKnock-out mouse modelProtein kinase signalingCortical cytoskeletonLoss of ezrinKinase signalingPlasma membraneCell migrationSignaling pathwayEzrinResponse to lipopolysaccharideTissue-resident macrophagesMouse modelLipopolysaccharideCytoskeletonEzrin expressionLung microenvironmentKinaseMonocyte recruitmentProteinAkt
2017
Ezrin links CFTR to TLR4 signaling to orchestrate anti-bacterial immune response in macrophages
Di Pietro C, Zhang PX, O’Rourke T, Murray TS, Wang L, Britto CJ, Koff JL, Krause DS, Egan ME, Bruscia EM. Ezrin links CFTR to TLR4 signaling to orchestrate anti-bacterial immune response in macrophages. Scientific Reports 2017, 7: 10882. PMID: 28883468, PMCID: PMC5589856, DOI: 10.1038/s41598-017-11012-7.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell LineCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorCytoskeletal ProteinsDisease Models, AnimalMacrophage ActivationMacrophagesMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPseudomonas aeruginosaPseudomonas InfectionsSignal TransductionToll-Like Receptor 4ConceptsCystic fibrosis transmembrane conductance regulatorPI3K/AktFibrosis transmembrane conductance regulatorTransmembrane conductance regulatorPI3K/Akt signalingConductance regulatorAnti-bacterial immune responseAkt signalingAltered localizationEzrinCystic fibrosis diseaseMφ activationAktProtein levelsFibrosis diseaseActivationImmune regulationPhagocytosisInductionDirect linkSignalingRegulatorImmune responseMΦMacrophages
2013
Reduced Caveolin-1 Promotes Hyperinflammation due to Abnormal Heme Oxygenase-1 Localization in Lipopolysaccharide-Challenged Macrophages with Dysfunctional Cystic Fibrosis Transmembrane Conductance Regulator
Zhang PX, Murray TS, Villella VR, Ferrari E, Esposito S, D'Souza A, Raia V, Maiuri L, Krause DS, Egan ME, Bruscia EM. Reduced Caveolin-1 Promotes Hyperinflammation due to Abnormal Heme Oxygenase-1 Localization in Lipopolysaccharide-Challenged Macrophages with Dysfunctional Cystic Fibrosis Transmembrane Conductance Regulator. The Journal Of Immunology 2013, 190: 5196-5206. PMID: 23606537, PMCID: PMC3711148, DOI: 10.4049/jimmunol.1201607.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAnimalsCaveolin 1Cells, CulturedChildChild, PreschoolCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorFemaleHeme Oxygenase-1HumansInflammationLipopolysaccharidesLung DiseasesMacrophagesMaleMembrane ProteinsMiceMice, KnockoutNasal PolypsReactive Oxygen SpeciesSignal TransductionToll-Like Receptor 4Young AdultConceptsCav-1 expressionHeme oxygenase-1Dysfunctional cystic fibrosis transmembrane conductance regulatorCystic fibrosis transmembrane conductance regulatorCell surfaceFibrosis transmembrane conductance regulatorProtein caveolin-1Cellular redox statusCell surface localizationCellular oxidative stateTransmembrane conductance regulatorHO-1 enzymePositive feed-forward loopCystic fibrosis macrophagesNegative regulatorCaveolin-1Conductance regulatorCell survivalHO-1 deliverySurface localizationRedox statusMΦ responsesHO-1/CO pathwayPathwayPotential target
2012
The GTPase Activity of FlhF Is Dispensable for Flagellar Localization, but Not Motility, in Pseudomonas aeruginosa
Schniederberend M, Abdurachim K, Murray TS, Kazmierczak BI. The GTPase Activity of FlhF Is Dispensable for Flagellar Localization, but Not Motility, in Pseudomonas aeruginosa. Journal Of Bacteriology 2012, 195: 1051-1060. PMID: 23264582, PMCID: PMC3571332, DOI: 10.1128/jb.02013-12.Peer-Reviewed Original ResearchConceptsFlagellar functionGTPase activityOpportunistic human pathogen Pseudomonas aeruginosaHuman pathogen Pseudomonas aeruginosaSignal recognition particlePathogen Pseudomonas aeruginosaSingle-cell assaysFlhF proteinFlagellar localizationFlagellar assemblyRecognition particleAbiotic environmentProtein dimerizationFlagellar rotationNucleotide bindingFlhFPoint mutantsSurface organellesSwimming motilityBacterial motilityP. aeruginosaBacillus subtilisPseudomonas aeruginosaEnzymatic activityHydrolytic activity
2009
Pseudomonas aeruginosa OspR is an oxidative stress sensing regulator that affects pigment production, antibiotic resistance and dissemination during infection
Lan L, Murray TS, Kazmierczak BI, He C. Pseudomonas aeruginosa OspR is an oxidative stress sensing regulator that affects pigment production, antibiotic resistance and dissemination during infection. Molecular Microbiology 2009, 75: 76-91. PMID: 19943895, PMCID: PMC2881571, DOI: 10.1111/j.1365-2958.2009.06955.x.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SubstitutionAnimalsAnti-Bacterial AgentsBeta-Lactam ResistanceBeta-LactamsFemaleGene DeletionGene Expression Regulation, BacterialGlutathione PeroxidaseHydrogen PeroxideMiceMice, Inbred C57BLModels, BiologicalMutagenesis, Site-DirectedOxidative StressPigments, BiologicalPneumoniaPseudomonas aeruginosaPseudomonas InfectionsQuorum SensingRepressor ProteinsSignal TransductionStress, PhysiologicalTyrosineVirulenceConceptsOxidative stress sensingCys-24Stress sensingPigment productionNull mutant strainOxidative stressSerine substitution mutantsGlobal regulatorPromoter DNASubstitution mutantsAdditional genesInside hostsQuorum sensingCys residuesMutant strainConstitutive expressionMultiple pathwaysRegulatory effectsBeta-lactam resistanceGenesSignificant inductionRegulatorTyrosine metabolismOSPRP. aeruginosa
2007
Pseudomonas aeruginosa chronic colonization in cystic fibrosis patients
Murray TS, Egan M, Kazmierczak BI. Pseudomonas aeruginosa chronic colonization in cystic fibrosis patients. Current Opinion In Pediatrics 2007, 19: 83-88. PMID: 17224667, DOI: 10.1097/mop.0b013e3280123a5d.Peer-Reviewed Original ResearchConceptsCystic fibrosis patientsChronic colonizationAcute infectionFibrosis patientsCystic fibrosisP. aeruginosaChronic pulmonary colonizationChronic pulmonary diseaseCystic fibrosis airwayHost immune systemMucoid P. aeruginosaP. aeruginosa behaviorCystic fibrosis lungPulmonary diseaseClinical benefitChronic infectionP. aeruginosa pathogenesisLeading causePulmonary colonizationNew therapiesImmune systemAggressive usePotential therapeuticsInfectionPatients