Featured Publications
Integrated Single-Cell Atlas of Endothelial Cells of the Human Lung
Schupp JC, Adams TS, Cosme C, Raredon MSB, Yuan Y, Omote N, Poli S, Chioccioli M, Rose KA, Manning EP, Sauler M, DeIuliis G, Ahangari F, Neumark N, Habermann AC, Gutierrez AJ, Bui LT, Lafyatis R, Pierce RW, Meyer KB, Nawijn MC, Teichmann SA, Banovich NE, Kropski JA, Niklason LE, Pe’er D, Yan X, Homer RJ, Rosas IO, Kaminski N. Integrated Single-Cell Atlas of Endothelial Cells of the Human Lung. Circulation 2021, 144: 286-302. PMID: 34030460, PMCID: PMC8300155, DOI: 10.1161/circulationaha.120.052318.Peer-Reviewed Original ResearchConceptsDifferential expression analysisPrimary lung endothelial cellsLung endothelial cellsCell typesMarker genesExpression analysisSingle-cell RNA sequencing dataCross-species analysisVenous endothelial cellsEndothelial marker genesSingle-cell atlasMarker gene setsRNA sequencing dataEndothelial cellsSubsequent differential expression analysisDifferent lung cell typesResident cell typesLung cell typesCellular diversityEndothelial cell typesCapillary endothelial cellsHuman lung endothelial cellsPhenotypic diversityEndothelial diversityIndistinguishable populations
2024
Noninvasive assessment of the lung inflammation-fibrosis axis by targeted imaging of CMKLR1
Mannes P, Adams T, Farsijani S, Barnes C, Latoche J, Day K, Nedrow J, Ahangari F, Kaminski N, Lee J, Tavakoli S. Noninvasive assessment of the lung inflammation-fibrosis axis by targeted imaging of CMKLR1. Science Advances 2024, 10: eadm9817. PMID: 38896611, PMCID: PMC11186491, DOI: 10.1126/sciadv.adm9817.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisFibrotic lung diseaseRisk stratificationMurine modelLung fibrosisLung diseaseModel of bleomycin-induced lung fibrosisBleomycin-induced lung fibrosisImaging biomarkersMurine model of bleomycin-induced lung fibrosisBronchoalveolar lavage cellsMonocyte-derived macrophagesPositron emission tomographyInflammatory endotypesPulmonary fibrosisLavage cellsPoor survivalNoninvasive assessmentTherapeutic monitoringEmission tomographyCMKLR1FibrosisClinical trajectoryLungLung regions
2023
Low CC16 mRNA Expression Levels in Bronchial Epithelial Cells Are Associated with Asthma Severity.
Li X, Guerra S, Ledford JG, Kraft M, Li H, Hastie AT, Castro M, Denlinger LC, Erzurum SC, Fahy JV, Gaston B, Israel E, Jarjour NN, Levy BD, Mauger DT, Moore WC, Zein J, Kaminski N, Wenzel SE, Woodruff PG, Meyers DA, Bleecker ER. Low CC16 mRNA Expression Levels in Bronchial Epithelial Cells Are Associated with Asthma Severity. American Journal Of Respiratory And Critical Care Medicine 2023, 207: 438-451. PMID: 36066606, PMCID: PMC9940145, DOI: 10.1164/rccm.202206-1230oc.Peer-Reviewed Original ResearchConceptsBronchial epithelial cellsMRNA expression levelsAsthma severityT2 biomarkersAsthma susceptibilityT2 inflammationExpression levelsSevere Asthma Research ProgramSystemic corticosteroid useLower pulmonary functionEpithelial cellsAsthma-related phenotypesCorticosteroid useAsthma exacerbationsPulmonary functionAsthma developmentAsthma endotypesAsthma progressionInflammation biomarkersInflammation genesHost defenseCC16Th2 genesSeverityBiomarkers
2022
Pseudohypoxic HIF pathway activation dysregulates collagen structure-function in human lung fibrosis
Brereton CJ, Yao L, Davies ER, Zhou Y, Vukmirovic M, Bell JA, Wang S, Ridley RA, Dean L, Andriotis OG, Conforti F, Brewitz L, Mohammed S, Wallis T, Tavassoli A, Ewing RM, Alzetani A, Marshall BG, Fletcher SV, Thurner PJ, Fabre A, Kaminski N, Richeldi L, Bhaskar A, Schofield CJ, Loxham M, Davies DE, Wang Y, Jones MG. Pseudohypoxic HIF pathway activation dysregulates collagen structure-function in human lung fibrosis. ELife 2022, 11: e69348. PMID: 35188460, PMCID: PMC8860444, DOI: 10.7554/elife.69348.Peer-Reviewed Original ResearchConceptsHIF pathway activationPathway activationLung fibrosisOxidative stressHuman lung fibrosisOxidative stress scoreFibrillar collagen synthesisHypoxia-inducible factor (HIF) pathway activationExtracellular matrixActive fibrogenesisFibrosisHuman fibrosisFibrosis tissueHIF activationStress scoresVivo studiesCollagen synthesisMesenchymal cellsCritical pathwaysDownstream activationNormal fibroblastsCritical regulatorHIFActivationHuman tissues
2021
Blood Transcriptomics Predicts Progression of Pulmonary Fibrosis and Associated Natural Killer Cells.
Huang Y, Oldham JM, Ma SF, Unterman A, Liao SY, Barros AJ, Bonham CA, Kim JS, Vij R, Adegunsoye A, Strek ME, Molyneaux PL, Maher TM, Herazo-Maya JD, Kaminski N, Moore BB, Martinez FJ, Noth I. Blood Transcriptomics Predicts Progression of Pulmonary Fibrosis and Associated Natural Killer Cells. American Journal Of Respiratory And Critical Care Medicine 2021, 204: 197-208. PMID: 33689671, PMCID: PMC8650792, DOI: 10.1164/rccm.202008-3093oc.Peer-Reviewed Original ResearchElevated plasma level of Pentraxin 3 is associated with emphysema and mortality in smokers
Zhang Y, Tedrow J, Nouraie M, Li X, Chandra D, Bon J, Kass DJ, Fuhrman CR, Leader JK, Duncan SR, Kaminski N, Sciurba FC. Elevated plasma level of Pentraxin 3 is associated with emphysema and mortality in smokers. Thorax 2021, 76: 335-342. PMID: 33479043, PMCID: PMC8249179, DOI: 10.1136/thoraxjnl-2020-215356.Peer-Reviewed Original ResearchConceptsAirflow obstructionPlasma levelsLung tissueEmphysema severitySmoking-related lung diseaseAssociation of lungExpiratory airflow obstructionFormer tobacco smokersLevels of PTX3PTX3 gene expressionElevated plasma levelsHyaluronic acid levelsBlood of subjectsPlasma PTX3PTX3 levelsLung functionTobacco exposureClinical outcomesTobacco smokersLung diseasePentraxin 3Predictive biomarkersPTX3 expressionLower riskDisease patterns
2020
Expression of SARS-CoV-2 receptor ACE2 and coincident host response signature varies by asthma inflammatory phenotype
Camiolo M, Gauthier M, Kaminski N, Ray A, Wenzel SE. Expression of SARS-CoV-2 receptor ACE2 and coincident host response signature varies by asthma inflammatory phenotype. Journal Of Allergy And Clinical Immunology 2020, 146: 315-324.e7. PMID: 32531372, PMCID: PMC7283064, DOI: 10.1016/j.jaci.2020.05.051.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAngiotensin-Converting Enzyme 2AsthmaBetacoronavirusBiomarkersBronchiBronchoalveolar Lavage FluidCohort StudiesCoronavirus InfectionsCOVID-19EosinophilsFemaleGene Expression ProfilingHumansInterferon Type IInterferon-gammaMaleMiddle AgedPandemicsPeptidyl-Dipeptidase APneumonia, ViralProtein Interaction MappingReceptors, VirusRisk FactorsSARS-CoV-2Severity of Illness IndexT-LymphocytesTranscriptomeUnited StatesConceptsCoronavirus disease 2019Severe coronavirus disease 2019Subset of patientsDisease 2019Risk factorsBronchial epitheliumAcute respiratory syndrome coronavirus 2 infectionSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infectionSevere acute respiratory syndrome coronavirus 2Syndrome coronavirus 2 infectionType 2 inflammatory biomarkersAcute respiratory syndrome coronavirus 2Receptor ACE2SARS-CoV-2 receptor ACE2Respiratory syndrome coronavirus 2Asthma inflammatory phenotypesLarge asthma cohortsLower peripheral bloodT cell-activating factorCoronavirus 2 infectionEnzyme 2 (ACE2) expressionHistory of hypertensionDiagnosis of asthmaBronchoalveolar lavage lymphocytesT cell recruitment
2019
Plasma mitochondrial DNA is associated with extrapulmonary sarcoidosis
Ryu C, Brandsdorfer C, Adams T, Hu B, Kelleher DW, Yaggi M, Manning EP, Walia A, Reeves B, Pan H, Winkler J, Minasyan M, Dela Cruz CS, Kaminski N, Gulati M, Herzog EL. Plasma mitochondrial DNA is associated with extrapulmonary sarcoidosis. European Respiratory Journal 2019, 54: 1801762. PMID: 31273041, PMCID: PMC8088542, DOI: 10.1183/13993003.01762-2018.Peer-Reviewed Original ResearchConceptsExtrapulmonary diseaseMitochondrial DNAExtracellular mtDNABAL fluidAlpha-1 antitrypsin deficiencyPlasma mitochondrial DNAPlasma of patientsAfrican AmericansExtrapulmonary sarcoidosisSarcoidosis cohortSarcoidosis subjectsScadding stageAfrican American descentClinical featuresClinical findingsGranulomatous diseaseHealthy controlsAntitrypsin deficiencyGenomic researchHigher oddsSarcoidosisAggressive phenotypeMechanistic basisDiseaseTherapeutic insightsIncreased monocyte count as a cellular biomarker for poor outcomes in fibrotic diseases: a retrospective, multicentre cohort study
Scott MKD, Quinn K, Li Q, Carroll R, Warsinske H, Vallania F, Chen S, Carns MA, Aren K, Sun J, Koloms K, Lee J, Baral J, Kropski J, Zhao H, Herzog E, Martinez FJ, Moore BB, Hinchcliff M, Denny J, Kaminski N, Herazo-Maya JD, Shah NH, Khatri P. Increased monocyte count as a cellular biomarker for poor outcomes in fibrotic diseases: a retrospective, multicentre cohort study. The Lancet Respiratory Medicine 2019, 7: 497-508. PMID: 30935881, PMCID: PMC6529612, DOI: 10.1016/s2213-2600(18)30508-3.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisAbsolute monocyte countMonocyte countImmune cell typesElectronic health recordsPoor outcomeHigh riskSystemic sclerosisMonocyte percentageHypertrophic cardiomyopathyHigh absolute monocyte countPeripheral blood mononuclear cell samplesComplete blood count valuesSpecific immune cell typesTransplant-free survivalMulticentre cohort studyHealth recordsHigh-risk patientsBlood count valuesSame clinical presentationHigher monocyte countMononuclear cell samplesRisk of mortalityCell types
2018
Regularized Latent Class Model for Joint Analysis of High-Dimensional Longitudinal Biomarkers and a Time-to-Event Outcome
Sun J, Herazo-Maya J, Molyneaux PL, Maher TM, Kaminski N, Zhao H. Regularized Latent Class Model for Joint Analysis of High-Dimensional Longitudinal Biomarkers and a Time-to-Event Outcome. Biometrics 2018, 75: 69-77. PMID: 30178494, DOI: 10.1111/biom.12964.Peer-Reviewed Original ResearchConceptsJoint latent class modelLongitudinal biomarkersExtensive simulation studyLatent class modelLongitudinal submodelJoint modeling methodSurvival submodelLikelihood approachSimulation studyClass modelEvent outcomesLatent classesModeling methodMembership modelRandom effectsModeling approachClassSubmodelsJoint analysisModelBootstrapUnique trajectoriesNovel biological insightsInferenceS100A12 as a marker of worse cardiac output and mortality in pulmonary hypertension
Tzouvelekis A, Herazo‐Maya J, Ryu C, Chu J, Zhang Y, Gibson KF, Adonteng‐Boateng P, Li Q, Pan H, Cherry B, Ahmad F, Ford HJ, Herzog EL, Kaminski N, Fares WH. S100A12 as a marker of worse cardiac output and mortality in pulmonary hypertension. Respirology 2018, 23: 771-779. PMID: 29611244, PMCID: PMC6047907, DOI: 10.1111/resp.13302.Peer-Reviewed Original ResearchConceptsPeripheral blood mononuclear cellsPH patientsPH cohortCardiac outputWorld Health Organization group 1Idiopathic pulmonary fibrosis patientsPulmonary hypertension patientsPulmonary fibrosis patientsBlood mononuclear cellsProtein serum concentrationsHigher S100A12Pulmonary hypertensionS100A12 levelsOverall mortalityHypertension patientsPrognostic valueValidation cohortMononuclear cellsPeripheral bloodSerum concentrationsInflammatory diseasesGroup 1PatientsFibrosis patientsS100A12
2017
Application of “Omics” and Systems Biology to Sarcoidosis Research
Crouser ED, Fingerlin TE, Yang IV, Maier LA, Nana-Sinkam P, Collman RG, Kaminski N. Application of “Omics” and Systems Biology to Sarcoidosis Research. Annals Of The American Thoracic Society 2017, 14: s445-s451. PMID: 29053026, PMCID: PMC5822413, DOI: 10.1513/annalsats.201707-567ot.Peer-Reviewed Original ResearchConceptsSystems biology researchBiology researchSystems biologyDistinct genetic mechanismsNumerous genetic mutationsField of sarcoidosisGenetic mechanismsDiverse clinical phenotypesOmicsMechanistic underpinningsComprehensive profilingPolygenic diseaseGenetic mutationsDiverse diseasesBiologyAdvanced computational approachesEnormous data setsComputational approachClinical phenotypeOrganismsPolygenicMutationsDisease-related mortalityPhenotypeLife-altering symptomsModified mesenchymal stem cells using miRNA transduction alter lung injury in a bleomycin model
Huleihel L, Sellares J, Cardenes N, Álvarez D, Faner R, Sakamoto K, Yu G, Kapetanaki MG, Kaminski N, Rojas M. Modified mesenchymal stem cells using miRNA transduction alter lung injury in a bleomycin model. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2017, 313: l92-l103. PMID: 28385811, PMCID: PMC5538868, DOI: 10.1152/ajplung.00323.2016.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersBleomycinBone Marrow CellsCollagenCytokinesDisease Models, AnimalFemaleGene Expression RegulationGene Regulatory NetworksHumansInterleukin-6Leukocyte Common AntigensLung InjuryMesenchymal Stem Cell TransplantationMesenchymal Stem CellsMice, Inbred C57BLMicroRNAsRNA, MessengerSurvival AnalysisTransduction, GeneticTransfectionWeight LossConceptsBone marrow-derived mesenchymal stem cellsMesenchymal stem cellsLung fibrosisLate administrationBleomycin modelMiR-154Different preclinical modelsStem cellsCD45-positive cellsMurine bleomycin modelMarrow-derived mesenchymal stem cellsInitial weight lossLower survival rateAshcroft scoreLung injuryBleomycin instillationFibrotic changesCytokine expressionMice groupsLung tissueOH-prolinePreclinical modelsProtective effectTreatment groupsSurvival rate
2016
Validation of the prognostic value of MMP‐7 in idiopathic pulmonary fibrosis
Tzouvelekis A, Herazo‐Maya J, Slade M, Chu J, Deiuliis G, Ryu C, Li Q, Sakamoto K, Ibarra G, Pan H, Gulati M, Antin‐Ozerkis D, Herzog EL, Kaminski N. Validation of the prognostic value of MMP‐7 in idiopathic pulmonary fibrosis. Respirology 2016, 22: 486-493. PMID: 27761978, PMCID: PMC5352520, DOI: 10.1111/resp.12920.Peer-Reviewed Original ResearchConceptsTransplant-free survivalIdiopathic pulmonary fibrosisMMP-7 concentrationsMatrix metalloproteinase-7IPF patientsCause mortalityPulmonary fibrosisHealthy controlsMultivariate Cox proportional hazards modelCox proportional hazards modelPulmonary function parametersVariable clinical courseBaseline pulmonary function parametersProportional hazards modelIPF biomarkersProgressive diseaseClinical coursePoor prognosisPrognostic valueVital capacityIndependent biomarkerLung capacityPrognostic thresholdPlasma concentrationsMortality risk
2015
Rationale and Design of the Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis (GRADS) Study. Sarcoidosis Protocol
Moller DR, Koth LL, Maier LA, Morris A, Drake W, Rossman M, Leader JK, Collman RG, Hamzeh N, Sweiss NJ, Zhang Y, O’Neal S, Senior RM, Becich M, Hochheiser HS, Kaminski N, Wisniewski SR, Gibson KF, Group* F. Rationale and Design of the Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis (GRADS) Study. Sarcoidosis Protocol. Annals Of The American Thoracic Society 2015, 12: 1561-1571. PMID: 26193069, PMCID: PMC4627423, DOI: 10.1513/annalsats.201503-172ot.Peer-Reviewed Original ResearchConceptsAlpha-1 antitrypsin deficiencyClinical courseLung microbiomeAntitrypsin deficiencyClinical heterogeneityPathobiology of sarcoidosisTremendous clinical heterogeneityObservational cohort studyPulmonary function testsSystemic inflammatory responsePeripheral blood changesDiagnosis of sarcoidosisSelf-administered questionnaireCohort studyBaseline visitBronchoalveolar lavageFunction testsGranulomatous inflammationSystemic diseaseSarcoidosis phenotypesUrine testingClinical bronchoscopyInflammatory responseSarcoidosis StudyPrognostic biomarkerOral immunotherapy with type V collagen in idiopathic pulmonary fibrosis
Wilkes DS, Chew T, Flaherty KR, Frye S, Gibson KF, Kaminski N, Klemsz MJ, Lange W, Noth I, Rothhaar K. Oral immunotherapy with type V collagen in idiopathic pulmonary fibrosis. European Respiratory Journal 2015, 45: 1393-1402. PMID: 25614165, DOI: 10.1183/09031936.00105314.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisIPF patientsPulmonary fibrosisHigh-dose cohortLow-dose cohortSerious adverse eventsPhase 1 studyProgressive lung diseaseType V collagenPrecision medicine approachMatrix metalloproteinase-7Acute exacerbationIPF trialsOral immunotherapyAdverse eventsPlacebo armLung functionPoor prognosisVital capacityLung diseaseImmune responsePatientsMetalloproteinase-7Potential efficacyMedicine approach
2014
Gene Expression in Relation to Exhaled Nitric Oxide Identifies Novel Asthma Phenotypes with Unique Biomolecular Pathways
Modena BD, Tedrow JR, Milosevic J, Bleecker ER, Meyers DA, Wu W, Bar-Joseph Z, Erzurum SC, Gaston BM, Busse WW, Jarjour NN, Kaminski N, Wenzel SE. Gene Expression in Relation to Exhaled Nitric Oxide Identifies Novel Asthma Phenotypes with Unique Biomolecular Pathways. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 1363-1372. PMID: 25338189, PMCID: PMC4294630, DOI: 10.1164/rccm.201406-1099oc.Peer-Reviewed Original ResearchConceptsEpithelial cell gene expressionCell gene expressionGene expressionAirway epithelial cell gene expressionGene expression patternsSevere Asthma Research ProgramActin cytoskeletonGene clusterGenomic studiesGene transcriptionGene pathwaysMolecular basisExpression patternsAsthma phenotypesWnt pathwayMicroarray platformGenesNovel pathwayPhenotypeBiomolecular pathwaysNeuronal functionPathwayUnadjusted p-valuesExpressionBiological characteristicsBlockade of the Programmed Death-1 Pathway Restores Sarcoidosis CD4+ T-Cell Proliferative Capacity
Braun NA, Celada LJ, Herazo-Maya JD, Abraham S, Shaginurova G, Sevin CM, Grutters J, Culver DA, Dworski R, Sheller J, Massion PP, Polosukhin VV, Johnson JE, Kaminski N, Wilkes DS, Oswald-Richter KA, Drake WP. Blockade of the Programmed Death-1 Pathway Restores Sarcoidosis CD4+ T-Cell Proliferative Capacity. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 560-571. PMID: 25073001, PMCID: PMC4214083, DOI: 10.1164/rccm.201401-0188oc.Peer-Reviewed Original ResearchConceptsPD-1 pathway blockadeT cell proliferative capacityPeripheral blood mononuclear cellsPD-L1 expressionPD-1 pathwayBlood mononuclear cellsT cell functionPathway blockadePD-L1Clinical outcomesLung diseaseMononuclear cellsControl subjectsProliferative capacityT cellsImmunohistochemistry analysisPD-1/PD-L1 expressionControl peripheral blood mononuclear cellsHealthy control peripheral blood mononuclear cellsHealthy control lungsIdiopathic lung diseaseSpontaneous clinical resolutionChronic lung diseaseHealthy control subjectsEffective therapeutic interventionsWnt Coreceptor Lrp5 Is a Driver of Idiopathic Pulmonary Fibrosis
Lam AP, Herazo-Maya JD, Sennello JA, Flozak AS, Russell S, Mutlu GM, Budinger GR, DasGupta R, Varga J, Kaminski N, Gottardi CJ. Wnt Coreceptor Lrp5 Is a Driver of Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 185-195. PMID: 24921217, PMCID: PMC4226053, DOI: 10.1164/rccm.201401-0079oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedAnimalsBeta CateninBiomarkersDisease ProgressionFemaleHumansIdiopathic Pulmonary FibrosisLeukocytes, MononuclearLow Density Lipoprotein Receptor-Related Protein-5Low Density Lipoprotein Receptor-Related Protein-6MaleMiceMice, KnockoutMiddle AgedProspective StudiesSeverity of Illness IndexSignal TransductionTransforming Growth Factor betaWnt ProteinsConceptsIdiopathic pulmonary fibrosisPeripheral blood mononuclear cellsBlood mononuclear cellsLung fibrosisPulmonary fibrosisDisease progressionMononuclear cellsDisease severityNull miceAlveolar type 2 cellsTGF-β productionWild-type miceActivation of TGFType 2 cellsWnt pathway inhibitorsWnt/β-catenin signalingWnt coreceptors LRP5Role of LRP5Bone marrow cellsLrp5 lossΒ-catenin signalingPatient selectionSmall molecular inhibitorsAdditional cohortFibrosisThe Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis
Huang LS, Mathew B, Li H, Zhao Y, Ma SF, Noth I, Reddy SP, Harijith A, Usatyuk PV, Berdyshev EV, Kaminski N, Zhou T, Zhang W, Zhang Y, Rehman J, Kotha SR, Gurney TO, Parinandi NL, Lussier YA, Garcia JG, Natarajan V. The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 1402-1415. PMID: 24779708, PMCID: PMC4098083, DOI: 10.1164/rccm.201310-1917oc.Peer-Reviewed Original ResearchMeSH Keywords1-Acylglycerol-3-Phosphate O-AcyltransferaseAcyltransferasesAnimalsBiomarkersCardiolipinsCohort StudiesDisease Models, AnimalHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLeukocytes, MononuclearMiceMitochondriaPredictive Value of TestsPulmonary FibrosisRNA, MessengerSensitivity and SpecificitySeverity of Illness IndexConceptsPeripheral blood mononuclear cellsIdiopathic pulmonary fibrosisPulmonary fibrosisMurine modelAlveolar epithelial cellsOverall survivalReactive oxygen species generationLysocardiolipin acyltransferaseOxygen species generationCarbon monoxide diffusion capacityRadiation-induced pulmonary fibrosisPulmonary function outcomesEpithelial cellsBlood mononuclear cellsPreclinical murine modelsNovel therapeutic approachesSpecies generationBleomycin challengeLung inflammationLung protectionPulmonary functionFunction outcomesLung fibrosisMononuclear cellsFibrotic lungs