2022
Lung Microenvironments and Disease Progression in Fibrotic Hypersensitivity Pneumonitis.
De Sadeleer LJ, McDonough JE, Schupp JC, Yan X, Vanstapel A, Van Herck A, Everaerts S, Geudens V, Sacreas A, Goos T, Aelbrecht C, Nawrot TS, Martens DS, Schols D, Claes S, Verschakelen JA, Verbeken EK, Ackermann M, Decottignies A, Mahieu M, Hackett TL, Hogg JC, Vanaudenaerde BM, Verleden SE, Kaminski N, Wuyts WA. Lung Microenvironments and Disease Progression in Fibrotic Hypersensitivity Pneumonitis. American Journal Of Respiratory And Critical Care Medicine 2022, 205: 60-74. PMID: 34724391, PMCID: PMC8865586, DOI: 10.1164/rccm.202103-0569oc.Peer-Reviewed Original ResearchConceptsFibrotic hypersensitivity pneumonitisIdiopathic pulmonary fibrosisHypersensitivity pneumonitisLung zonesMolecular traitsUnused donor lungsInterstitial lung diseaseLocal disease extentProgression of fibrosisSevere fibrosis groupGene co-expression network analysisCo-expression network analysisExplant lungsDonor lungsLung involvementEndothelial functionLung findingsDisease extentPulmonary fibrosisLung diseaseFibrosis groupLung microenvironmentClinical behaviorDisease progressionBAL samples
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 Research
2020
Genetic analyses identify GSDMB associated with asthma severity, exacerbations, and antiviral pathways
Li X, Christenson SA, Modena B, Li H, Busse WW, Castro M, Denlinger LC, Erzurum SC, Fahy JV, Gaston B, Hastie AT, Israel E, Jarjour NN, Levy BD, Moore WC, Woodruff PG, Kaminski N, Wenzel SE, Bleecker ER, Meyers DA, Program N. Genetic analyses identify GSDMB associated with asthma severity, exacerbations, and antiviral pathways. Journal Of Allergy And Clinical Immunology 2020, 147: 894-909. PMID: 32795586, PMCID: PMC7876167, DOI: 10.1016/j.jaci.2020.07.030.Peer-Reviewed Original ResearchConceptsExpression quantitative trait loci (eQTL) analysisQuantitative trait locus (QTL) analysisSingle nucleotide polymorphismsGasdermin BMultiple single nucleotide polymorphismsFunctional genesExpression levelsLocus analysisAntiviral pathwaysGenes/single-nucleotide polymorphismsWhole genome sequencesGene expression dataEpithelial cellsImmune system pathwaysHigh expression levelsHuman bronchial epithelial cellsIFN regulatory factorGPI attachmentGSDMB expressionAsthma susceptibilityGenetic analysisGene expressionPathway analysisBronchial epithelial cellsRegulatory factors
2019
Transcriptional regulatory model of fibrosis progression in the human lung
McDonough JE, Ahangari F, Li Q, Jain S, Verleden SE, Herazo-Maya J, Vukmirovic M, DeIuliis G, Tzouvelekis A, Tanabe N, Chu F, Yan X, Verschakelen J, Homer RJ, Manatakis DV, Zhang J, Ding J, Maes K, De Sadeleer L, Vos R, Neyrinck A, Benos PV, Bar-Joseph Z, Tantin D, Hogg JC, Vanaudenaerde BM, Wuyts WA, Kaminski N. Transcriptional regulatory model of fibrosis progression in the human lung. JCI Insight 2019, 4 PMID: 31600171, PMCID: PMC6948862, DOI: 10.1172/jci.insight.131597.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisAdvanced fibrosisAlveolar surface densityFibrosis progressionLung fibrosisHuman lungDynamic Regulatory Events MinerExtent of fibrosisIPF lungsPulmonary fibrosisControl lungsIPF tissueB lymphocytesFibrosisLungLinear mixed-effects modelsMixed-effects modelsGene expression changesSystems biology modelsDifferential gene expression analysisGene expression analysisProgressionGene expression networksRNA sequencingBiology models
2017
Local and Systemic CD4+ T Cell Exhaustion Reverses with Clinical Resolution of Pulmonary Sarcoidosis
Hawkins C, Shaginurova G, Shelton DA, Herazo-Maya JD, Oswald-Richter KA, Rotsinger JE, Young A, Celada LJ, Kaminski N, Sevin C, Drake WP. Local and Systemic CD4+ T Cell Exhaustion Reverses with Clinical Resolution of Pulmonary Sarcoidosis. Journal Of Immunology Research 2017, 2017: 3642832. PMID: 29234685, PMCID: PMC5695030, DOI: 10.1155/2017/3642832.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedApoptosisCD4-Positive T-LymphocytesCell ProliferationCells, CulturedClonal AnergyCytokinesDisease ProgressionFemaleGene Expression RegulationHumansLymphocyte ActivationMaleMiddle AgedProgrammed Cell Death 1 ReceptorReceptors, Antigen, T-Cell, alpha-betaSarcoidosis, PulmonaryTh1 CellsYoung AdultConceptsT cell exhaustionTh1 cytokine expressionPD-1 expressionCell exhaustionCytokine expressionT cellsHealthy controlsInhibitory cell surface receptorsT cell immune functionTh1 immune responseChronic antigenic stimulationCell immune functionProliferative capacityT cell functionSarcoidosis subjectsSystemic CD4Pulmonary sarcoidosisDisease resolutionProgressive diseaseClinical resolutionCytokine productionAntigenic stimulationDisease progressionImmune responseCD4
2015
Update in Diffuse Parenchymal Lung Disease 2013
Rosas IO, Kaminski N. Update in Diffuse Parenchymal Lung Disease 2013. American Journal Of Respiratory And Critical Care Medicine 2015, 191: 270-274. PMID: 25635490, PMCID: PMC4351573, DOI: 10.1164/rccm.201405-0856up.Peer-Reviewed Original ResearchMeSH KeywordsAnti-Inflammatory Agents, Non-SteroidalClinical Trials, Phase III as TopicDisease ProgressionDrug ApprovalEnzyme InhibitorsGenomicsHumansIdiopathic Pulmonary FibrosisIndolesLung Diseases, InterstitialPolymorphism, GeneticPyridonesTreatment OutcomeUnited StatesUnited States Food and Drug AdministrationConceptsMajority of patientsDistinct clinical presentationsSignificant clinical implicationsClinical presentationPulmonary fibrosis researchDisease progressionClinical implicationsGenetic biomarkersPatientsFibrosis researchGenetic variantsBiological mechanismsIPFNew biological mechanismsNintedanibPirfenidonePeriodHistoric approval
2014
Wnt 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 cohortFibrosisC-X-C Motif Chemokine 13 (CXCL13) Is a Prognostic Biomarker of Idiopathic Pulmonary Fibrosis
Vuga LJ, Tedrow JR, Pandit KV, Tan J, Kass DJ, Xue J, Chandra D, Leader JK, Gibson KF, Kaminski N, Sciurba FC, Duncan SR. C-X-C Motif Chemokine 13 (CXCL13) Is a Prognostic Biomarker of Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 966-974. PMID: 24628285, PMCID: PMC4098096, DOI: 10.1164/rccm.201309-1592oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overBiomarkersCase-Control StudiesChemokine CXCL13Disease ProgressionEnzyme-Linked Immunosorbent AssayFemaleHumansIdiopathic Pulmonary FibrosisImmunohistochemistryMaleMiddle AgedOligonucleotide Array Sequence AnalysisPredictive Value of TestsPrognosisPulmonary Disease, Chronic ObstructiveRisk FactorsSensitivity and SpecificitySeverity of Illness IndexConceptsChronic obstructive pulmonary diseaseC motif chemokine 13IPF lungsPrognostic biomarkerB cellsIdiopathic pulmonary fibrosis (IPF) pathogenesisB cell-targeted therapiesAntibody-mediated syndromeDysregulated B cellsPulmonary fibrosis pathogenesisPulmonary artery hypertensionObstructive pulmonary diseaseIdiopathic pulmonary fibrosisSix-month survivalB-cell traffickingAcute exacerbationArtery hypertensionCXCL13 mRNAPlasma CXCL13IPF pathogenesisRespiratory failureLung injuryCXCL13 concentrationsPulmonary diseaseRadiographic emphysema
2013
Idiopathic Pulmonary Fibrosis: Time to Get Personal?
Noth I, Kaminski N. Idiopathic Pulmonary Fibrosis: Time to Get Personal? American Journal Of Respiratory And Critical Care Medicine 2013, 188: 1392-1394. PMID: 24328772, PMCID: PMC3917381, DOI: 10.1164/rccm.201311-1956ed.Peer-Reviewed Original ResearchSerum lysyl oxidase-like 2 levels and idiopathic pulmonary fibrosis disease progression.
Chien JW, Richards TJ, Gibson KF, Zhang Y, Lindell KO, Shao L, Lyman SK, Adamkewicz JI, Smith V, Kaminski N, O'Riordan T. Serum lysyl oxidase-like 2 levels and idiopathic pulmonary fibrosis disease progression. European Respiratory Journal 2013, 43: 1430-8. PMID: 24177001, DOI: 10.1183/09031936.00141013.Peer-Reviewed Original ResearchConceptsIPF disease progressionDisease progressionIdiopathic pulmonary fibrosis patientsCarbon monoxide diffusion capacityPulmonary fibrosis patientsDisease progression eventsGAP subjectsIPF studiesPathological stromaVital capacityLOXL2 levelsProgression eventsDiffusion capacityFibrosis patientsSpirometric dataDisease severityPhysiological surrogatesProgressionPatientsRiskMultiple limitationsSubjectsLevelsProteomic analysisCohort
2010
The pulmonary histopathologic manifestations of the anti-Jo-1 tRNA synthetase syndrome
Yousem SA, Gibson K, Kaminski N, Oddis CV, Ascherman DP. The pulmonary histopathologic manifestations of the anti-Jo-1 tRNA synthetase syndrome. Modern Pathology 2010, 23: 874-880. PMID: 20228783, DOI: 10.1038/modpathol.2010.65.Peer-Reviewed Original ResearchConceptsInterstitial lung diseaseDiffuse alveolar damageNonspecific interstitial pneumoniaUsual interstitial pneumoniaInterstitial pneumoniaSynthetase syndromeAlveolar damageNative lungPulmonary interstitial lung diseaseUsual interstitial pneumonia patternChronic interstitial lung diseaseTRNA synthetase autoantibodiesTRNA synthetase syndromeIdiopathic inflammatory myopathiesPercent of patientsSurgical lung biopsyInterstitial pneumonia patternChronic interstitial pneumoniaConnective tissue disordersAutoimmune groupInterstitial injuryAcute decompensationOrganizing pneumoniaInflammatory myopathiesLung biopsy
2009
Impact of a disease-management program on symptom burden and health-related quality of life in patients with idiopathic pulmonary fibrosis and their care partners
Lindell KO, Olshansky E, Song MK, Zullo TG, Gibson KF, Kaminski N, Hoffman LA. Impact of a disease-management program on symptom burden and health-related quality of life in patients with idiopathic pulmonary fibrosis and their care partners. Heart & Lung 2009, 39: 304-313. PMID: 20561836, PMCID: PMC3467095, DOI: 10.1016/j.hrtlng.2009.08.005.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PsychologicalAgedAnalysis of VarianceAnxietyCaregiversDepressionDisease ManagementDisease ProgressionFemaleHealth Status IndicatorsHumansIdiopathic Pulmonary FibrosisMalePilot ProjectsPsychometricsQuality of LifeRespiratory Function TestsStress, PsychologicalSurveys and QuestionnairesUnited StatesConceptsDisease management interventionsAdvanced lung diseaseHealth-related qualityIdiopathic pulmonary fibrosisSymptom burdenLung diseaseCare partnersPulmonary fibrosisExperimental group participantsTime of diagnosisInterstitial lung diseaseExperimental group patientsGroup participantsPittsburgh Medical CenterDisease management programsPulmonary fibrosis resultsGroup patientsRespiratory failureUsual careMedian survivalIntervention groupPatient participantsMedical CenterFibrosis resultsPatients
2007
Accelerated Variant of Idiopathic Pulmonary Fibrosis: Clinical Behavior and Gene Expression Pattern
Selman M, Carrillo G, Estrada A, Mejia M, Becerril C, Cisneros J, Gaxiola M, Pérez-Padilla R, Navarro C, Richards T, Dauber J, King TE, Pardo A, Kaminski N. Accelerated Variant of Idiopathic Pulmonary Fibrosis: Clinical Behavior and Gene Expression Pattern. PLOS ONE 2007, 2: e482. PMID: 17534432, PMCID: PMC1868965, DOI: 10.1371/journal.pone.0000482.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisMonths of symptomsSubset of patientsRapid progressorsPulmonary fibrosisProgression of IPFBronchoalveolar lavage (BAL) cellular profileActive matrix metalloproteinase-9Kaplan-Meyer methodRapid progressor groupTime of diagnosisBeginning of symptomsEnd-stage diseaseAccelerated clinical courseMatrix metalloproteinase-9Proportional hazards modelMigration/proliferationAdenosine 2B receptorSmooth muscle cellsAlveolar epithelial cellsIPF patientsProgressor groupSlow progressorsClinical courseInsidious onset
2003
Loss of integrin αvβ6-mediated TGF-β activation causes Mmp12-dependent emphysema
Morris DG, Huang X, Kaminski N, Wang Y, Shapiro SD, Dolganov G, Glick A, Sheppard D. Loss of integrin αvβ6-mediated TGF-β activation causes Mmp12-dependent emphysema. Nature 2003, 422: 169-173. PMID: 12634787, DOI: 10.1038/nature01413.Peer-Reviewed Original ResearchConceptsTGF-β activationLungs of miceActive TGF-β1Pulmonary gene expressionHeterodimeric cell-surface proteinsTransgenic expressionPulmonary emphysemaMMP12 expressionTGF-β1Functional alterationsΒ6 integrinIntegrin αvβ6Latent TGFMarked inductionEmphysemaGrowth factorMacrophage metalloelastaseCell surface proteinsActivation pathwayMiceTGFActivationCell growthIntegrinsExpression