2024
CCR2+ monocytes are dispensable to resolve acute pulmonary Pseudomonas aeruginosa infections in WT and Cystic Fibrosis mice
Öz H, Braga C, Gudneppanavar R, Di Pietro C, Huang P, Zhang P, Krause D, Egan M, Murray T, Bruscia E. CCR2+ monocytes are dispensable to resolve acute pulmonary Pseudomonas aeruginosa infections in WT and Cystic Fibrosis mice. Journal Of Leukocyte Biology 2024, qiae218. PMID: 39365279, DOI: 10.1093/jleuko/qiae218.Peer-Reviewed Original ResearchLung tissue damageCystic fibrosisTissue damageMonocyte recruitmentImmune responsePulmonary Pseudomonas aeruginosa infectionHyper-inflammatory immune responseCystic fibrosis micePropagate tissue damagePseudomonas aeruginosaLungs of patientsChronic neutrophilic inflammationImmunological response to infectionHost immune responseMonocyte-derived macrophagesTarget monocyte recruitmentSite of injuryResponse to infectionCFTR modulatorsPA infectionChronic inflammatory disease conditionsReduced bactericidal activityAdjunctive therapyClinical outcomesEradicate infection
2022
Recruited monocytes/macrophages drive pulmonary neutrophilic inflammation and irreversible lung tissue remodeling in cystic fibrosis
Öz H, Cheng E, Di Pietro C, Tebaldi T, Biancon G, Zeiss C, Zhang P, Huang P, Esquibies S, Britto C, Schupp J, Murray T, Halene S, Krause D, Egan M, Bruscia E. Recruited monocytes/macrophages drive pulmonary neutrophilic inflammation and irreversible lung tissue remodeling in cystic fibrosis. Cell Reports 2022, 41: 111797. PMID: 36516754, PMCID: PMC9833830, DOI: 10.1016/j.celrep.2022.111797.Peer-Reviewed Original ResearchConceptsC motif chemokine receptor 2Monocytes/macrophagesLung tissue damageCystic fibrosisTissue damageCF lungPulmonary neutrophilic inflammationPro-inflammatory environmentChemokine receptor 2CF lung diseaseNumber of monocytesSpecific therapeutic agentsGrowth factor βCF transmembrane conductance regulatorLung hyperinflammationLung neutrophiliaNeutrophilic inflammationNeutrophil inflammationInflammation contributesLung damageNeutrophil recruitmentLung diseaseLung tissueReceptor 2Therapeutic targetRecruitment of monocytes primed to express heme oxygenase-1 ameliorates pathological lung inflammation in cystic fibrosis
Di Pietro C, Öz HH, Zhang PX, Cheng EC, Martis V, Bonfield TL, Kelley TJ, Jubin R, Abuchowski A, Krause DS, Egan ME, Murray TS, Bruscia EM. Recruitment of monocytes primed to express heme oxygenase-1 ameliorates pathological lung inflammation in cystic fibrosis. Experimental & Molecular Medicine 2022, 54: 639-652. PMID: 35581352, PMCID: PMC9166813, DOI: 10.1038/s12276-022-00770-8.Peer-Reviewed Original ResearchConceptsHeme oxygenase-1Cystic fibrosisOxygenase-1Myeloid differentiation factor 88Neutrophilic pulmonary inflammationChronic airway infectionDifferentiation factor 88HO-1 levelsDisease mouse modelPseudomonas aeruginosaRecruitment of monocytesResolution of inflammationMonocytes/macrophagesTreatment of CFConditional knockout miceMechanism of actionLung neutrophiliaNeutrophilic inflammationLung inflammationAirway infectionPulmonary diseasePulmonary inflammationFactor 88Lung damageProinflammatory cytokines
2016
Increased susceptibility of Cftr−/− mice to LPS-induced lung remodeling
Bruscia E, Zhang P, Barone C, Scholte BJ, Homer R, Krause D, Egan ME. Increased susceptibility of Cftr−/− mice to LPS-induced lung remodeling. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2016, 310: l711-l719. PMID: 26851259, PMCID: PMC4836110, DOI: 10.1152/ajplung.00284.2015.Peer-Reviewed Original ResearchConceptsLung pathologyCF miceImmune responseWT miceChronic inflammationCystic fibrosisAbnormal immune responseChronic pulmonary infectionPersistent immune responseWild-type littermatesCF mouse modelsPseudomonas aeruginosa lipopolysaccharideCF lung pathologyPulmonary infectionChronic administrationLPS exposurePersistent inflammationLung remodelingWT littermatesLung tissueOverall pathologyMouse modelInflammationChronic exposureBacterial products
2008
Macrophages Directly Contribute to the Exaggerated Inflammatory Response in Cystic Fibrosis Transmembrane Conductance Regulator−/− Mice
Bruscia EM, Zhang PX, Ferreira E, Caputo C, Emerson JW, Tuck D, Krause DS, Egan ME. Macrophages Directly Contribute to the Exaggerated Inflammatory Response in Cystic Fibrosis Transmembrane Conductance Regulator−/− Mice. American Journal Of Respiratory Cell And Molecular Biology 2008, 40: 295-304. PMID: 18776130, PMCID: PMC2645527, DOI: 10.1165/rcmb.2008-0170oc.Peer-Reviewed Original ResearchConceptsExaggerated inflammatory responseExaggerated immune responseBone marrow-derived macrophagesIL-6Marrow-derived macrophagesCystic fibrosisCF miceKeratinocyte chemoattractantCytokine responsesInflammatory responseIL-1alphaImmune responseAlveolar macrophagesBronchoalveolar lavage fluidGranulocyte colony-stimulating factorNumber of neutrophilsChemoattractant protein-1CF lung diseaseElevated cytokine responseInnate immune systemImportant therapeutic targetCF mouse modelsPopulation of macrophagesColony-stimulating factorPseudomonas aeruginosa LPSRectal Potential Difference and the Functional Expression of CFTR in the Gastrointestinal Epithelia in Cystic Fibrosis Mouse Models
Weiner SA, Caputo C, Bruscia E, Ferreira EC, Price JE, Krause DS, Egan ME. Rectal Potential Difference and the Functional Expression of CFTR in the Gastrointestinal Epithelia in Cystic Fibrosis Mouse Models. Pediatric Research 2008, 63: 73-78. PMID: 18043508, DOI: 10.1203/pdr.0b013e31815b4bc6.Peer-Reviewed Original ResearchConceptsRectal potential differenceMouse modelCF mouse modelsCystic fibrosisFibrosis mouse modelDifferent mouse modelsCystic fibrosis mouse modelUssing chamber methodEffects of interventionsAutosomal recessive diseasePharmacologic interventionsRespiratory epitheliumElectrophysiologic phenotypeGastrointestinal epitheliumCF transmembrane conductance regulator (CFTR) geneRecessive diseaseVivo methodsVivo assaysVivo dataCFTR functionTransmembrane conductance regulator geneReliable assayEpitheliumInterventionCFTR expression