2023
Single-Cell Rna Sequencing of the Mouse Isograft and Allograft Lung after Orthotopic Lung Transplantation
Hooft C, Kaes J, Heigl T, Beeckmans H, Kerckhof P, Vanstapel A, Jin X, Slambrouck J, Vandervelde C, Van Raemdonck D, Kaminski N, McDonough J, Ceulemans L, Vos R, Vanaudenaerde B. Single-Cell Rna Sequencing of the Mouse Isograft and Allograft Lung after Orthotopic Lung Transplantation. The Journal Of Heart And Lung Transplantation 2023, 42: s539. DOI: 10.1016/j.healun.2023.02.1473.Peer-Reviewed Original ResearchLung transplantationImmune cellsImmune responseEndothelial cellsMouse lung transplant modelSingle-cell RNA sequencingCell RNA sequencingLung transplant modelOrthotopic lung transplantationAdaptive immune cellsInnate immune cellsRNA sequencingSingle-cell RNA profilingAllograft lungChronic rejectionInnate inflammationTransplant modelEndothelial upregulationMHC expressionPrimary onsetSham controlsSingle cell suspensionsWeek 10Week 1Transplantation
2021
Prediction of Survival after Chronic Lung Allograft Dysfunction in Lung Transplant Recipients by Blood Profiling Using a Predefined 52 Gene Signature
Luijk B, Krebber M, Li Q, Kardol-Hoefnagel T, Budding K, van Kessel D, Grutters J, Otten H, Kaminski N, Maya J. Prediction of Survival after Chronic Lung Allograft Dysfunction in Lung Transplant Recipients by Blood Profiling Using a Predefined 52 Gene Signature. The Journal Of Heart And Lung Transplantation 2021, 40: s155-s156. DOI: 10.1016/j.healun.2021.01.470.Peer-Reviewed Original ResearchChronic lung allograft dysfunctionDiagnosis of CLADPeripheral blood mononuclear cellsLung allograft dysfunctionAllograft dysfunctionLTx recipientsRisk groupsHigh riskRisk scoreIdiopathic pulmonary fibrosis patientsLung transplant recipientsHigh-risk patientsKaplan-Meier analysisPulmonary fibrosis patientsBlood mononuclear cellsHigh-risk groupLow-risk groupLow-risk scoresPrediction of survivalLong-term survivalCLAD onsetCLAD patientsLung transplantationTransplant recipientsOverall survival
2020
Cathepsin B promotes collagen biosynthesis, which drives bronchiolitis obliterans syndrome
Morrone C, Smirnova NF, Jeridi A, Kneidinger N, Hollauer C, Schupp JC, Kaminski N, Jenne D, Eickelberg O, Yildirim AÖ. Cathepsin B promotes collagen biosynthesis, which drives bronchiolitis obliterans syndrome. European Respiratory Journal 2020, 57: 2001416. PMID: 33303550, DOI: 10.1183/13993003.01416-2020.Peer-Reviewed Original ResearchConceptsBronchoalveolar lavage fluidCathepsin B activityHealthy donorsLung tissueCollagen depositionB activityCathepsin BBronchiolitis obliterans syndromeProgression of BOSFluorescence resonance energy transfer-based assayPromising therapeutic targetGrowth factor-β1Cathepsin B levelsSubsequent collagen depositionBOS pathogenesisBOS patientsBOS progressionLTx patientsLymphocytic bronchiolitisObliterans syndromeLung transplantationPeribronchial fibrosisPulmonary dysfunctionLung functionMajor complicationsSmall airways pathology in idiopathic pulmonary fibrosis: a retrospective cohort study
Verleden SE, Tanabe N, McDonough JE, Vasilescu DM, Xu F, Wuyts WA, Piloni D, De Sadeleer L, Willems S, Mai C, Hostens J, Cooper JD, Verbeken EK, Verschakelen J, Galban CJ, Van Raemdonck DE, Colby TV, Decramer M, Verleden GM, Kaminski N, Hackett TL, Vanaudenaerde BM, Hogg JC. Small airways pathology in idiopathic pulmonary fibrosis: a retrospective cohort study. The Lancet Respiratory Medicine 2020, 8: 573-584. PMID: 32061334, PMCID: PMC7292784, DOI: 10.1016/s2213-2600(19)30356-x.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisSevere idiopathic pulmonary fibrosisUnused donor lungsRetrospective cohort studyTerminal bronchiolesMultidetector CTCohort studyDonor lungsPulmonary fibrosisIPF tissueLung tissueMinimal fibrosisVideo-assisted thoracic surgical biopsyDiagnosis of IPFAshcroft fibrosis scoreMultidisciplinary consensus committeeStructural lung injuryInflammatory immune cellsExpiratory flow rateLow lung volumesPotential therapeutic targetMicro-CTLung transplantationVisible airwaysIPF group
2013
Peripheral Blood Mononuclear Cell Gene Expression Profiles Predict Poor Outcome in Idiopathic Pulmonary Fibrosis
Herazo-Maya JD, Noth I, Duncan SR, Kim S, Ma SF, Tseng GC, Feingold E, Juan-Guardela BM, Richards TJ, Lussier Y, Huang Y, Vij R, Lindell KO, Xue J, Gibson KF, Shapiro SD, Garcia JG, Kaminski N. Peripheral Blood Mononuclear Cell Gene Expression Profiles Predict Poor Outcome in Idiopathic Pulmonary Fibrosis. Science Translational Medicine 2013, 5: 205ra136. PMID: 24089408, PMCID: PMC4175518, DOI: 10.1126/scitranslmed.3005964.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkersCD28 AntigensCD4 AntigensCluster AnalysisCohort StudiesGene Expression ProfilingHumansIdiopathic Pulmonary FibrosisLeukocytes, MononuclearOligonucleotide Array Sequence AnalysisReproducibility of ResultsReverse Transcriptase Polymerase Chain ReactionSignal TransductionTreatment OutcomeConceptsTransplant-free survivalIdiopathic pulmonary fibrosisPeripheral blood mononuclear cell gene expression profilesReplication cohortCell gene expression profilesPoor outcomePulmonary fibrosisQuantitative reverse transcription polymerase chain reactionReverse transcription-polymerase chain reactionProportional hazards modelTranscription-polymerase chain reactionGene expression profilesPotential cellular sourcesT cell activationIPF patientsLung transplantationMicroarray cohortPatient ageOutcome biomarkerPatient groupVital capacityPolymerase chain reactionT cellsDiscovery cohortITK expression
2012
Retinoic Acid–related Orphan Receptor-α Is Induced in the Setting of DNA Damage and Promotes Pulmonary Emphysema
Shi Y, Cao J, Gao J, Zheng L, Goodwin A, An CH, Patel A, Lee JS, Duncan SR, Kaminski N, Pandit KV, Rosas IO, Choi AM, Morse D. Retinoic Acid–related Orphan Receptor-α Is Induced in the Setting of DNA Damage and Promotes Pulmonary Emphysema. American Journal Of Respiratory And Critical Care Medicine 2012, 186: 412-419. PMID: 22744720, PMCID: PMC5450975, DOI: 10.1164/rccm.201111-2023oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersCells, CulturedDisease Models, AnimalDNA DamageDNA RepairGene Expression ProfilingHumansLungMiceMice, Inbred C57BLMice, Neurologic MutantsNuclear Receptor Subfamily 1, Group F, Member 1Oligonucleotide Array Sequence AnalysisPulmonary Disease, Chronic ObstructivePulmonary EmphysemaTobacco Smoke PollutionConceptsRetinoic acid-related orphan receptorAcid-related orphan receptorCigarette smoke extractLungs of patientsPathogenesis of emphysemaRORA expressionCigarette smokeAirspace enlargementSmoke extractCigarette smoke exposureSmoke-induced emphysemaOrphan receptorDNA damageActive smokingLung transplantationSmoke exposureLung cancerPulmonary emphysemaLung tissueEmphysemaPatientsGene expression profilingApoptotic cell deathMiceEnhanced susceptibility
2011
The HLA Class II Allele DRB1*1501 Is Over-Represented in Patients with Idiopathic Pulmonary Fibrosis
Xue J, Gochuico BR, Alawad AS, Feghali-Bostwick CA, Noth I, Nathan SD, Rosen GD, Rosas IO, Dacic S, Ocak I, Fuhrman CR, Cuenco KT, Smith MA, Jacobs SS, Zeevi A, Morel PA, Pilewski JM, Valentine VG, Gibson KF, Kaminski N, Sciurba FC, Zhang Y, Duncan SR. The HLA Class II Allele DRB1*1501 Is Over-Represented in Patients with Idiopathic Pulmonary Fibrosis. PLOS ONE 2011, 6: e14715. PMID: 21373184, PMCID: PMC3044131, DOI: 10.1371/journal.pone.0014715.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisIPF patientsIPF subjectsAmbulatory patientsPulmonary fibrosisLung diseaseHLA-DRB1Normal subjectsEtiology of IPFHuman leukocyte antigen (HLA) allele frequenciesManifestations of IPFAbnormal adaptive immune responsesLung transplantation recipientsHLA class IIAdaptive immune responsesU.S. medical centersHLA-DR locusNormal reference populationDistinct clinical phenotypesRefractory lung diseaseSpecific HLA-DRB1Lung transplantationTransplant recipientsTransplantation recipientsGrim prognosis
2009
Systemic Inhibition of NF-κB Activation Protects from Silicosis
Di Giuseppe M, Gambelli F, Hoyle GW, Lungarella G, Studer SM, Richards T, Yousem S, McCurry K, Dauber J, Kaminski N, Leikauf G, Ortiz LA. Systemic Inhibition of NF-κB Activation Protects from Silicosis. PLOS ONE 2009, 4: e5689. PMID: 19479048, PMCID: PMC2682759, DOI: 10.1371/journal.pone.0005689.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCytokinesEpithelial CellsFemaleGene Expression RegulationGenes, DominantHumansI-kappa B ProteinsLungLung TransplantationMacrophagesMaleMiceMice, Inbred C57BLMiddle AgedNF-kappa BNF-KappaB Inhibitor alphaNitrilesPrognosisRNA, MessengerSilicon DioxideSilicosisSulfonesTumor Necrosis Factor-alphaConceptsNF-kappaB activationLung transplantationSystemic inhibitionLung injuryCollagen depositionLung transplant databaseIdiopathic pulmonary fibrosisComplex lung diseaseNecrosis factor alphaPathogenesis of silicosisIkappaB-alpha phosphorylationInnate immune responsePotential therapeutic strategyNF-kappaB inhibitionMouse experimental modelIPF patientsLung graftsGraft rejectionOverall survivalSurvival benefitTransplant databasePulmonary fibrosisPoor outcomeInflammatory cellsLung disease
2008
Malignancy in Lung Transplantation: Biomarkers, Gender Differences, and Consideration of a Systems Biology Approach
Studer SM, Taioli E, Crespo M, Kaminski N. Malignancy in Lung Transplantation: Biomarkers, Gender Differences, and Consideration of a Systems Biology Approach. Transplantation 2008, 85: s69-s71. PMID: 18425041, DOI: 10.1097/tp.0b013e31816c2feb.Peer-Reviewed Original Research