2021
Transcriptomics of bronchoalveolar lavage cells identifies new molecular endotypes of sarcoidosis
Vukmirovic M, Yan X, Gibson KF, Gulati M, Schupp JC, DeIuliis G, Adams TS, Hu B, Mihaljinec A, Woolard TN, Lynn H, Emeagwali N, Herzog EL, Chen ES, Morris A, Leader JK, Zhang Y, Garcia JGN, Maier LA, Collman RG, Drake WP, Becich MJ, Hochheiser H, Wisniewski SR, Benos PV, Moller DR, Prasse A, Koth LL, Kaminski N. Transcriptomics of bronchoalveolar lavage cells identifies new molecular endotypes of sarcoidosis. European Respiratory Journal 2021, 58: 2002950. PMID: 34083402, PMCID: PMC9759791, DOI: 10.1183/13993003.02950-2020.Peer-Reviewed Original ResearchMeSH KeywordsBronchoalveolar LavageBronchoalveolar Lavage FluidHumansSarcoidosisSarcoidosis, PulmonaryTranscriptomeConceptsWeighted gene co-expression network analysisGene co-expression network analysisCo-expression network analysisGene expression programsGene expression patternsDistinct transcriptional programsImmune response pathwaysIon Torrent ProtonMicroarray expression datasetsExpression programsTranscriptional programsPhenotypic traitsGene modulesResponse pathwaysRNA sequencingMolecular endotypesExpression patternsGene expressionHilar lymphadenopathyOrgan involvementGenomic researchMechanistic targetExpression datasetsT helper type 1T cell immune responses
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 insights
2017
Microbes Are Associated with Host Innate Immune Response in Idiopathic Pulmonary Fibrosis
Huang Y, Ma SF, Espindola MS, Vij R, Oldham JM, Huffnagle GB, Erb-Downward JR, Flaherty KR, Moore BB, White ES, Zhou T, Li J, Lussier YA, Han MK, Kaminski N, Garcia JG, Hogaboam CM, Martinez FJ, Noth I. Microbes Are Associated with Host Innate Immune Response in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2017, 196: 208-219. PMID: 28157391, PMCID: PMC5519968, DOI: 10.1164/rccm.201607-1525oc.Peer-Reviewed Original ResearchConceptsProgression-free survivalMicrobial diversityRegulated signaling pathwaysNOD-like receptor signalingRNA sequencing dataGene expression dataMicroarray gene expression dataImmune response pathwaysMicrobial interactionsMicrobial communitiesHost innate immune responseResponse pathwaysLung microbial communityLeukocyte phenotypeImmune responseSequencing dataNetwork analysisShannon indexSignaling pathwaysToll-like receptor 9 stimulationExpression associationsExpression dataIndividual generaIdiopathic pulmonary fibrosis progressionOligomerization domain
2015
Rationale and Design of the Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis Study. Alpha-1 Protocol
Strange C, Senior RM, Sciurba F, O’Neal S, Morris A, Wisniewski SR, Bowler R, Hochheiser HS, Becich MJ, Zhang Y, Leader JK, Methé BA, Kaminski N, Sandhaus RA, Group* F. Rationale and Design of the Genomic Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis Study. Alpha-1 Protocol. Annals Of The American Thoracic Society 2015, 12: 1551-1560. PMID: 26153726, PMCID: PMC4627425, DOI: 10.1513/annalsats.201503-143oc.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAlpha 1-Antitrypsin DeficiencyBronchoalveolar LavageCross-Sectional StudiesExercise ToleranceFemaleGenomicsGenotypeHumansMaleMicrobiotaMiddle AgedPhenotypeProspective StudiesPulmonary Disease, Chronic ObstructivePulmonary EmphysemaResearch DesignRespiratory Function TestsSarcoidosisTomography, X-Ray ComputedConceptsAlpha-1 antitrypsin deficiencyAugmentation therapyBronchoalveolar lavageAntitrypsin deficiencyClinical presentationPiZZ individualsAlpha-1-antitrypsin augmentation therapyAlpha-1 antitrypsin genotypeChronic obstructive pulmonary disease phenotypesPulmonary function testingAge 35 yearsVariable clinical presentationCross-sectional studyAlpha-1 antitrypsinIntermediate outcome measuresPulmonary disease phenotypesUnique genetic causeExercise capacityTherapeutic trialsChest tomographyClinical symptomsCOPD pathogenesisCOPD phenotypesFunction testingCOPD StudyRationale 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 biomarker
2013
Activation of Human Mesenchymal Stem Cells Impacts Their Therapeutic Abilities in Lung Injury by Increasing Interleukin (IL)-10 and IL-1RN Levels
Bustos ML, Huleihel L, Meyer EM, Donnenberg AD, Donnenberg VS, Sciurba JD, Mroz L, McVerry BJ, Ellis BM, Kaminski N, Rojas M. Activation of Human Mesenchymal Stem Cells Impacts Their Therapeutic Abilities in Lung Injury by Increasing Interleukin (IL)-10 and IL-1RN Levels. Stem Cells Translational Medicine 2013, 2: 884-895. PMID: 24089414, PMCID: PMC3808203, DOI: 10.5966/sctm.2013-0033.Peer-Reviewed Original ResearchConceptsAcute respiratory distress syndromeAnti-inflammatory effectsBone marrow aspirateReceptor antagonistMarrow aspiratesMesenchymal stem cellsBronchoalveolar lavage inflammatory cellsIL-1 receptor antagonistHuman mesenchymal stem cellsLung injury scoreRespiratory distress syndromeAnti-inflammatory capacityExpression of interleukinStem cellsARDS patientsLung inflammationLung injuryDistress syndromeEndotoxemic micePulmonary edemaInflammatory cellsInjury scoreClinical trialsEffective therapyImmunomodulatory phenotypeSyndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling
Shi Y, Gochuico BR, Yu G, Tang X, Osorio JC, Fernandez IE, Risquez CF, Patel AS, Shi Y, Wathelet MG, Goodwin AJ, Haspel JA, Ryter SW, Billings EM, Kaminski N, Morse D, Rosas IO. Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling. American Journal Of Respiratory And Critical Care Medicine 2013, 188: 831-841. PMID: 23924348, PMCID: PMC3826270, DOI: 10.1164/rccm.201303-0434oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBleomycinBronchoalveolar LavageCaveolin 1Disease Models, AnimalGene Expression ProfilingGenetic MarkersHumansHydroxyprolineIdiopathic Pulmonary FibrosisIn Vitro TechniquesMacrophages, AlveolarMiceMice, TransgenicSignal TransductionSyndecan-2Tissue Array AnalysisTransforming Growth Factor beta1Up-RegulationConceptsHuman syndecan-2TGF-β1 target genesSyndecan-2Target genesIdiopathic pulmonary fibrosisEpithelial cell apoptosisAlveolar epithelial cellsEpithelial cellsTransforming Growth Factor-β1 SignalingCell apoptosisAntifibrotic effectsTGF-β1TGF-β signalingLung injuryPulmonary fibrosisAlveolar epithelial cell apoptosisExtracellular matrix productionTransgenic miceGrowth factor-β1 (TGF-β1) signalingMacrophage-specific overexpressionLung fibrosisMicroarray assayΒ1 signalingAlveolar macrophagesDownstream expression
2008
Oxidative Stress Alters Syndecan-1 Distribution in Lungs with Pulmonary Fibrosis*
Kliment CR, Englert JM, Gochuico BR, Yu G, Kaminski N, Rosas I, Oury TD. Oxidative Stress Alters Syndecan-1 Distribution in Lungs with Pulmonary Fibrosis*. Journal Of Biological Chemistry 2008, 284: 3537-3545. PMID: 19073610, PMCID: PMC2635035, DOI: 10.1074/jbc.m807001200.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisLavage fluidNeutrophil chemotaxisSyndecan-1EC-SODSyndecan-1 ectodomainWound healingMouse lungNull miceWestern blotOxidative stressInterstitial lung diseaseBronchoalveolar lavage fluidShed syndecan-1Aberrant wound healingAlveolar epithelial cellsHuman lung samplesHuman syndecan-1Extracellular superoxide dismutaseEpithelial wound healingIPF lungsProgressive fibrosisLung fibrosisAlveolar epithelial wound healing