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
Nebulized Hyaluronan Ameliorates lung inflammation in cystic fibrosis mice
Gavina M, Luciani A, Villella VR, Esposito S, Ferrari E, Bressani I, Casale A, Bruscia EM, Maiuri L, Raia V. Nebulized Hyaluronan Ameliorates lung inflammation in cystic fibrosis mice. Pediatric Pulmonology 2012, 48: 761-771. PMID: 22825912, DOI: 10.1002/ppul.22637.Peer-Reviewed Original ResearchConceptsLung inflammationCystic fibrosisLung tissueReactive oxygen speciesScnn1b-Tg miceHuman airway epithelial cellsSaline-treated miceChronic lung inflammationInflammatory protein-2Chronic respiratory diseasesPeroxisome Proliferator-Activated Receptor GammaPotential anti-inflammatory drugsAnti-inflammatory drugsAirway epithelial cellsCystic fibrosis miceIB3-1Myeloperoxidase levelsMIP-2MPO activityMacrophage infiltrationFibrosis miceTumor necrosisExogenous administrationTNFα expressionCF airwaysThe Carbon Monoxide Releasing Molecule CORM-2 Attenuates Pseudomonas aeruginosa Biofilm Formation
Murray TS, Okegbe C, Gao Y, Kazmierczak BI, Motterlini R, Dietrich LE, Bruscia EM. The Carbon Monoxide Releasing Molecule CORM-2 Attenuates Pseudomonas aeruginosa Biofilm Formation. PLOS ONE 2012, 7: e35499. PMID: 22563385, PMCID: PMC3338523, DOI: 10.1371/journal.pone.0035499.Peer-Reviewed Original ResearchMeSH KeywordsAnti-Bacterial AgentsBiofilmsCarbon MonoxideEpithelial CellsHumansOrganometallic CompoundsPseudomonas aeruginosaPseudomonas InfectionsReactive Oxygen SpeciesTobramycinConceptsCORM-2 treatmentP. aeruginosa lung infectionP. aeruginosaAeruginosa lung infectionCORM-2Clinical P. aeruginosaMolecule CORM-2Current antimicrobial agentsChronic infectionLung infectionNew therapiesRelated infectionsNon-mucoid strainsReactive oxygen speciesInfectionNovel therapeutic propertiesTherapeutic propertiesAntimicrobial agentsAdditive effectPseudomonas aeruginosaBiofilm formationOxygen speciesTreatmentAeruginosa