2018
BPIFA1 regulates lung neutrophil recruitment and interferon signaling during acute inflammation
Britto CJ, Niu N, Khanal S, Huleihel L, Herazo-Maya J, Thompson A, Sauler M, Slade MD, Sharma L, Dela Cruz CS, Kaminski N, Cohn LE. BPIFA1 regulates lung neutrophil recruitment and interferon signaling during acute inflammation. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2018, 316: l321-l333. PMID: 30461288, PMCID: PMC6397348, DOI: 10.1152/ajplung.00056.2018.Peer-Reviewed Original ResearchConceptsLung inflammationAcute inflammationC motif chemokine ligand 10Lung neutrophil recruitmentRegulation of CXCL10Acute lung inflammationBronchoalveolar lavage concentrationsChemokine ligand 10Innate immune responseIFN regulatory factorIntranasal LPSLavage concentrationsLung recruitmentNeutrophil recruitmentWT miceImmune effectsLung diseasePMN recruitmentInflammatory responseLPS treatmentLung tissueInflammatory signalsImmune responseImmunomodulatory propertiesInflammationBPI Fold-Containing Family A Member 1 (BPIFA1) regulates lung neutrophil recruitment and interferon signaling during acute inflammation
Khanal S, Niu N, Huleihel L, Herazo-Maya J, Kaminski N, Cohn L, Britto C. BPI Fold-Containing Family A Member 1 (BPIFA1) regulates lung neutrophil recruitment and interferon signaling during acute inflammation. 2018, pa4254. DOI: 10.1183/13993003.congress-2018.pa4254.Peer-Reviewed Original ResearchClub Cell Protein-16 modifies airway inflammation in asthma and is associated with significant clinical asthma outcomes
Kraft M, Ledford J, Gozdz J, Li X, Francisco D, Manne A, Guerra S, Martinez F, Kaminski N, Wenzel S, Meyers D, Bleecker E. Club Cell Protein-16 modifies airway inflammation in asthma and is associated with significant clinical asthma outcomes. 2018, pa5496. DOI: 10.1183/13993003.congress-2018.pa5496.Peer-Reviewed Original Research
2015
Suppression of NLRX1 in chronic obstructive pulmonary disease
Kang MJ, Yoon CM, Kim BH, Lee CM, Zhou Y, Sauler M, Homer R, Dhamija A, Boffa D, West AP, Shadel GS, Ting JP, Tedrow JR, Kaminski N, Kim WJ, Lee CG, Oh YM, Elias JA. Suppression of NLRX1 in chronic obstructive pulmonary disease. Journal Of Clinical Investigation 2015, 125: 2458-2462. PMID: 25938787, PMCID: PMC4497738, DOI: 10.1172/jci71747.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseObstructive pulmonary diseaseCigarette smokeAlveolar destructionPulmonary diseaseHuman chronic obstructive pulmonary diseaseExpression of NLRX1Innate immune pathwaysInnate immune responseQuality of lifeCOPD patientsPulmonary functionSubsequent inflammationImmune responseInflammasome activationMurine modelIndependent cohortImmune pathwaysInflammationDisease severityInflammasome responseImportant mediatorCell apoptosisNLRX1Tissue effects
2013
Gene expression profiles reveal molecular mechanisms involved in the progression and resolution of bleomycin-induced lung fibrosis
Cabrera S, Selman M, Lonzano-Bolaños A, Konishi K, Richards TJ, Kaminski N, Pardo A. Gene expression profiles reveal molecular mechanisms involved in the progression and resolution of bleomycin-induced lung fibrosis. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2013, 304: l593-l601. PMID: 23457188, PMCID: PMC4116413, DOI: 10.1152/ajplung.00320.2012.Peer-Reviewed Original ResearchConceptsLung fibrosisFibrotic responseResolution of bleomycinTranscriptional signatureGene expression profilesGene microarray analysisC57BL/6 miceProminent inflammationSingle doseExtracellular matrix-related genesInitial progressionControl animalsTIMP-1Normal architectureExpression profilesFibrosisMatrix metalloproteinasesHydroxyproline contentBleomycinMatrix-related genesSubsequent resolutionProgressionInflammationEqual volumeMicroarray analysis
2011
Cytokine-Like Factor I (CLF1) Expression Is Increased In Idiopathic Pulmonary Fibrosis (IPF) And Promotes Inflammation But Decreases Fibrosis In Bleomycin Injury
Kass D, Loh K, Borczuk A, Tedrow J, Guardela B, Kaminski N, Greenberg S. Cytokine-Like Factor I (CLF1) Expression Is Increased In Idiopathic Pulmonary Fibrosis (IPF) And Promotes Inflammation But Decreases Fibrosis In Bleomycin Injury. 2011, a2710-a2710. DOI: 10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2710.Peer-Reviewed Original Research
2002
Gene-microarray analysis of multiple sclerosis lesions yields new targets validated in autoimmune encephalomyelitis
Lock C, Hermans G, Pedotti R, Brendolan A, Schadt E, Garren H, Langer-Gould A, Strober S, Cannella B, Allard J, Klonowski P, Austin A, Lad N, Kaminski N, Galli SJ, Oksenberg JR, Raine CS, Heller R, Steinman L. Gene-microarray analysis of multiple sclerosis lesions yields new targets validated in autoimmune encephalomyelitis. Nature Medicine 2002, 8: 500-508. PMID: 11984595, DOI: 10.1038/nm0502-500.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsAutopsyChronic DiseaseEncephalomyelitis, Autoimmune, ExperimentalFemaleGranulocyte Colony-Stimulating FactorHumansInflammationInterferon-gammaInterleukin-17Interleukin-6MiceMice, Inbred C57BLMultiple SclerosisOligonucleotide Array Sequence AnalysisReceptors, FcReproducibility of ResultsTranscription, GeneticConceptsExperimental autoimmune encephalomyelitisMultiple sclerosis lesionsMS lesionsAutoimmune encephalomyelitisSclerosis lesionsGranulocyte colony-stimulating factorCommon γ chainColony-stimulating factorGene microarray analysisAcute phaseInflammatory cytokinesInterleukin-6Chronic diseasesLesionsNew targetsEncephalomyelitisTherapyDownstream pathwaysMicroarray analysisΓ-chainMicroarray studiesInflammationChronicCytokinesInterferon
2000
Global analysis of gene expression in pulmonary fibrosis reveals distinct programs regulating lung inflammation and fibrosis
Kaminski N, Allard J, Pittet J, Zuo F, Griffiths M, Morris D, Huang X, Sheppard D, Heller R. Global analysis of gene expression in pulmonary fibrosis reveals distinct programs regulating lung inflammation and fibrosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 1778-1783. PMID: 10677534, PMCID: PMC26512, DOI: 10.1073/pnas.97.4.1778.Peer-Reviewed Original ResearchConceptsPulmonary fibrosisLung inflammationBleomycin administrationSusceptible miceMultiple time pointsFibrotic responseFibrosisFibrotic diseasesInflammationMore effective strategiesGene expressionTime pointsMiceBeta6 subunitMolecular mechanismsSequential inductionGene expression patternsExpression patternsNull mutationResponseEffective strategyLungExpressionBleomycinGene expression programs
1999
A Mechanism for Regulating Pulmonary Inflammation and Fibrosis: The Integrin αvβ6 Binds and Activates Latent TGF β1
Munger J, Huang X, Kawakatsu H, Griffiths M, Dalton S, Wu J, Pittet J, Kaminski N, Garat C, Matthay M, Rifkin D, Sheppard D. A Mechanism for Regulating Pulmonary Inflammation and Fibrosis: The Integrin αvβ6 Binds and Activates Latent TGF β1. Cell 1999, 96: 319-328. PMID: 10025398, DOI: 10.1016/s0092-8674(00)80545-0.Peer-Reviewed Original ResearchMeSH Keywords3T3 CellsAnimalsAntigens, NeoplasmBleomycinCHO CellsCricetinaeEpithelial CellsEsophagusHumansIntegrinsKeratinocytesLigandsMiceMice, KnockoutPeptide FragmentsProtein BindingProtein PrecursorsProteinsPulmonary FibrosisTransforming Growth Factor betaTransforming Growth Factor beta1Tumor Cells, CulturedConceptsLatency-associated peptideIntegrin alpha v beta 6Alpha v beta 6 integrinAlpha v beta 6Beta gene productsTGF beta 1Latent TGF-β1TGF-beta functionGrowth factor-beta (TGF-beta) family membersPulmonary inflammationExaggerated inflammationPulmonary fibrosisTGF-β1Beta 6Alpha vBeta 1Beta family membersInflammationFibrosisFamily membersNovel mechanismExtracellular activationVivoActivationIntegrins