2023
microRNA-33 deficiency in macrophages enhances autophagy, improves mitochondrial homeostasis, and protects against lung fibrosis
Ahangari F, Price N, Malik S, Chioccioli M, Bärnthaler T, Adams T, Kim J, Pradeep S, Ding S, Cosme C, Rose K, McDonough J, Aurelien N, Ibarra G, Omote N, Schupp J, DeIuliis G, Nunez J, Sharma L, Ryu C, Dela Cruz C, Liu X, Prasse A, Rosas I, Bahal R, Fernandez-Hernando C, Kaminski N. microRNA-33 deficiency in macrophages enhances autophagy, improves mitochondrial homeostasis, and protects against lung fibrosis. JCI Insight 2023, 8: e158100. PMID: 36626225, PMCID: PMC9977502, DOI: 10.1172/jci.insight.158100.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutophagyBleomycinHomeostasisHumansIdiopathic Pulmonary FibrosisMacrophagesMiceMicroRNAsMitochondriaConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisMiR-33MiR-33 levelsSpecific genetic ablationBronchoalveolar lavage cellsNovel therapeutic approachesMitochondrial homeostasisFatty acid metabolismMacrophages protectsBleomycin injuryLavage cellsLung fibrosisHealthy controlsInflammatory responseTherapeutic approachesImmunometabolic responsesCholesterol effluxFibrosisFatal diseasePharmacological inhibitionSterol regulatory element-binding protein (SREBP) genesGenetic ablationMacrophagesEx vivo mouse
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 target
2019
The value of bronchoalveolar lavage for discrimination between healthy and diseased individuals
Frye B, Schupp J, Rothe M, Köhler T, Prasse A, Zissel G, Vach W, Müller‐Quernheim J. The value of bronchoalveolar lavage for discrimination between healthy and diseased individuals. Journal Of Internal Medicine 2019, 287: 54-65. PMID: 31612575, DOI: 10.1111/joim.12973.Peer-Reviewed Original Research
2013
Lung Collagens Perpetuate Pulmonary Fibrosis via CD204 and M2 Macrophage Activation
Stahl M, Schupp J, Jäger B, Schmid M, Zissel G, Müller-Quernheim J, Prasse A. Lung Collagens Perpetuate Pulmonary Fibrosis via CD204 and M2 Macrophage Activation. PLOS ONE 2013, 8: e81382. PMID: 24278429, PMCID: PMC3835428, DOI: 10.1371/journal.pone.0081382.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisAlveolar macrophagesCollagen type IHealthy donorsInterleukin-1 receptor antagonistType IM2 macrophage activationExpression of CCL2Lower respiratory tractIL-1ra productionAbundant collagen productionInnate immune responsePhospho-Akt expressionType I effectsExpression of CD204Collagen breakdown productsBronchoalveolar lavageReceptor antagonistCD204 expressionRespiratory tractLung collagenImmune responseM2 typeMacrophage activation