2022
FK506-Binding Protein 11 Is a Novel Plasma Cell-Specific Antibody Folding Catalyst with Increased Expression in Idiopathic Pulmonary Fibrosis
Preisendörfer S, Ishikawa Y, Hennen E, Winklmeier S, Schupp JC, Knüppel L, Fernandez IE, Binzenhöfer L, Flatley A, Juan-Guardela BM, Ruppert C, Guenther A, Frankenberger M, Hatz RA, Kneidinger N, Behr J, Feederle R, Schepers A, Hilgendorff A, Kaminski N, Meinl E, Bächinger HP, Eickelberg O, Staab-Weijnitz CA. FK506-Binding Protein 11 Is a Novel Plasma Cell-Specific Antibody Folding Catalyst with Increased Expression in Idiopathic Pulmonary Fibrosis. Cells 2022, 11: 1341. PMID: 35456020, PMCID: PMC9027113, DOI: 10.3390/cells11081341.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPlasma cellsPulmonary fibrosisIgG antibodiesFatal chronic lung diseaseCell linesAntibody-producing plasma cellsChronic lung diseaseAdaptive immune responsesHybridoma cell linesAlveolar epithelial cell lineCell-specific antibodiesCell deathAntibody-producing hybridoma cellsAutoimmune featuresX-box-binding protein 1IPF lungsLung diseaseEpithelial cell lineImmune responseLymphatic tissueB cellsStress-mediated cell deathAntibody secretionER stress-mediated cell death
2021
Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity
Bui LT, Winters NI, Chung MI, Joseph C, Gutierrez AJ, Habermann AC, Adams TS, Schupp JC, Poli S, Peter LM, Taylor CJ, Blackburn JB, Richmond BW, Nicholson AG, Rassl D, Wallace WA, Rosas IO, Jenkins RG, Kaminski N, Kropski JA, Banovich NE. Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity. Nature Communications 2021, 12: 4314. PMID: 34262047, PMCID: PMC8280215, DOI: 10.1038/s41467-021-24467-0.Peer-Reviewed Original ResearchConceptsChronic lung diseaseLung diseaseImmune responseSARS-CoV-2 entry factorsSevere coronavirus disease-19SARS-CoV-2 infectionWorse COVID-19 outcomesSARS-CoV-2 entryAdaptive immune responsesCoronavirus disease-19COVID-19 outcomesInnate immune responseInflammatory gene expression programSimilar cellular distributionPoor outcomePeripheral lungViral exposureDisease-19Inflammatory microenvironmentEntry factorsLung epitheliumLung cellsViral replicationAT2 cellsBasal differences
2014
Blockade 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 interventions
2010
Have advanced research technologies made real impact on respiratory medicine?
Kjetil A, EICKELBERG O, GAULDIE J, KAMINSKI N, Martin K. Have advanced research technologies made real impact on respiratory medicine? Respirology 2010, 15: 876-880. PMID: 20646243, DOI: 10.1111/j.1440-1843.2010.01811.x.Peer-Reviewed Original ResearchConceptsGene array analysisGenetic manipulationGene expressionSystems biologyMolecular researchNovel pathwayArray analysisTremendous sophisticationDisease initiationPotential roleNovel toolAdvanced research technologiesLung diseaseRespiratory medicineHumans todayProteomicsUnique insightsGenesRNABiologyBioinformaticsProteinChronic lung diseaseTherapeutic interventionsPathway
2009
Chronic lung diseases
Wu W, Kaminski N. Chronic lung diseases. WIREs Mechanisms Of Disease 2009, 1: 298-308. PMID: 20835999, DOI: 10.1002/wsbm.23.Peer-Reviewed Original ResearchConceptsSystems biology approachBiology approachChronic lung diseaseComplex human diseasesHigh-throughput technologiesLung diseaseSystems biologyHuman diseasesTraditional experimental approachesComplex lung diseaseBiomedical researchExperimental approachSerious economic burdenHigh morbiditySerious threatHuman healthEconomic burdenMortality rateDiseaseBiologyMicroarrayPromising findingsIncreased local expression of coagulation factor X contributes to the fibrotic response in human and murine lung injury
Scotton CJ, Krupiczojc MA, Königshoff M, Mercer PF, Lee YC, Kaminski N, Morser J, Post JM, Maher TM, Nicholson AG, Moffatt JD, Laurent GJ, Derian CK, Eickelberg O, Chambers RC. Increased local expression of coagulation factor X contributes to the fibrotic response in human and murine lung injury. Journal Of Clinical Investigation 2009, 119: 2550-2563. PMID: 19652365, PMCID: PMC2735922, DOI: 10.1172/jci33288.Peer-Reviewed Original ResearchMeSH KeywordsActinsAdultAgedAnimalsBase SequenceBleomycinCase-Control StudiesCell DifferentiationCells, CulturedFactor XaFactor Xa InhibitorsFemaleFibroblastsGene ExpressionHumansIdiopathic Pulmonary FibrosisLung InjuryMaleMiceMice, Inbred C57BLMiddle AgedModels, BiologicalPulmonary FibrosisReceptor, PAR-1Receptors, VitronectinRNA, MessengerTransforming Growth Factor betaUp-RegulationConceptsProteinase-activated receptor 1Lung injuryPulmonary fibrosisFibrotic responseCoagulation cascade contributesExcessive procoagulant activityChronic lung diseaseIdiopathic pulmonary fibrosisMurine lung injuryDirect FXa inhibitorsFibrotic lung tissueHuman adult lungFactor XTGF-beta activationNovel pathogenetic mechanismLung biopsyMicrovascular leakFibrotic fociLung diseaseFibrosis developmentLung tissuePathogenetic mechanismsAlpha-SMATissue injuryAlveolar epitheliumClara Cells Attenuate the Inflammatory Response through Regulation of Macrophage Behavior
Snyder JC, Reynolds SD, Hollingsworth JW, Li Z, Kaminski N, Stripp BR. Clara Cells Attenuate the Inflammatory Response through Regulation of Macrophage Behavior. American Journal Of Respiratory Cell And Molecular Biology 2009, 42: 161-171. PMID: 19423773, PMCID: PMC2822978, DOI: 10.1165/rcmb.2008-0353oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChronic DiseaseFemaleIn Vitro TechniquesInterleukin-6LipopolysaccharidesLung DiseasesMacrophages, AlveolarMaleMiceMice, CongenicMice, Inbred C57BLMice, KnockoutNeutrophilsOligonucleotide Array Sequence AnalysisPneumoniaRNA, MessengerSignal TransductionToll-Like Receptor 4Tumor Necrosis Factor-alphaUteroglobinConceptsClara cell secretory proteinChronic lung diseaseCell secretory functionWild-type miceInflammatory responseClara cellsLung diseaseEpithelial remodelingGene expression analysisSecretory functionMacrophage behaviorTNF-alpha signalingLung inflammatory responsePolymorphonuclear leukocyte recruitmentTNF-alpha productionExpression analysisSecretory proteinsGenetic mouse modelsPseudomonas aeruginosa LPSPathway modelingCCSP deficiencyLung inflammationExcessive inflammationTNF-alphaAirway fluid
2008
MMP1 and MMP7 as Potential Peripheral Blood Biomarkers in Idiopathic Pulmonary Fibrosis
Rosas IO, Richards TJ, Konishi K, Zhang Y, Gibson K, Lokshin AE, Lindell KO, Cisneros J, MacDonald SD, Pardo A, Sciurba F, Dauber J, Selman M, Gochuico BR, Kaminski N. MMP1 and MMP7 as Potential Peripheral Blood Biomarkers in Idiopathic Pulmonary Fibrosis. PLOS Medicine 2008, 5: e93. PMID: 18447576, PMCID: PMC2346504, DOI: 10.1371/journal.pmed.0050093.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisInterstitial lung diseaseSubclinical interstitial lung diseasePulmonary fibrosisLung diseaseIPF patientsChronic progressive fibrotic lung diseaseControl individualsAsymptomatic interstitial lung diseaseProgressive fibrotic lung diseaseChronic obstructive pulmonary diseasePotential peripheral blood biomarkerChronic hypersensitivity pneumonitisPeripheral blood biomarkersChronic lung diseaseObstructive pulmonary diseaseFibrotic lung diseaseBronchoalveolar lavage fluidIndependent validation cohortFamilial pulmonary fibrosisProtein signaturesPulmonary diseaseSubstantial morbidityHypersensitivity pneumonitisLavage fluid