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
2018
Hypercapnia increases airway smooth muscle contractility via caspase-7–mediated miR-133a–RhoA signaling
Shigemura M, Lecuona E, Angulo M, Homma T, Rodríguez DA, Gonzalez-Gonzalez FJ, Welch LC, Amarelle L, Kim SJ, Kaminski N, Budinger GRS, Solway J, Sznajder JI. Hypercapnia increases airway smooth muscle contractility via caspase-7–mediated miR-133a–RhoA signaling. Science Translational Medicine 2018, 10 PMID: 30185650, PMCID: PMC6889079, DOI: 10.1126/scitranslmed.aat1662.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAgedAged, 80 and overAirway ResistanceAnimalsCalciumCalpainCarbon DioxideCaspase 7Chronic DiseaseDown-RegulationEnzyme ActivationFemaleHumansHypercapniaMaleMEF2 Transcription FactorsMice, Inbred C57BLMicroRNAsMiddle AgedMuscle ContractionMuscle, SmoothMyocytes, Smooth MusclePulmonary Disease, Chronic ObstructiveRhoA GTP-Binding ProteinSignal TransductionConceptsChronic obstructive pulmonary diseaseAirway smooth muscle cellsSmooth muscle cellsMouse airway smooth muscle cellsSevere chronic obstructive pulmonary diseaseHuman airway smooth muscle cellsAirway smooth muscle contractilityMuscle cellsCorrection of hypercapniaSmooth muscle cell contractionCohort of patientsObstructive pulmonary diseaseHigh airway resistanceSevere lung diseaseDevelopment of hypercapniaSmooth muscle contractilityMuscle cell contractionRas homolog family member AMyosin light chain phosphorylationAirway contractilityAirway contractionHypercapnic patientsCOPD severityPulmonary diseaseAirway resistance
2013
Oral Antimycobacterial Therapy in Chronic Cutaneous Sarcoidosis: A Randomized, Single-Masked, Placebo-Controlled Study
Drake WP, Oswald-Richter K, Richmond BW, Isom J, Burke VE, Algood H, Braun N, Taylor T, Pandit KV, Aboud C, Yu C, Kaminski N, Boyd AS, King LE. Oral Antimycobacterial Therapy in Chronic Cutaneous Sarcoidosis: A Randomized, Single-Masked, Placebo-Controlled Study. JAMA Dermatology 2013, 149: 1040-1049. PMID: 23863960, PMCID: PMC3927541, DOI: 10.1001/jamadermatol.2013.4646.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, OralAdultAgedAnti-Bacterial AgentsAzithromycinCD4-Positive T-LymphocytesChronic DiseaseDrug Therapy, CombinationEthambutolFemaleFollow-Up StudiesHumansLevofloxacinMaleMiddle AgedOfloxacinRifampinSarcoidosisSeverity of Illness IndexSingle-Blind MethodSkin DiseasesTranscriptomeTreatment OutcomeYoung AdultConceptsChronic cutaneous sarcoidosisCutaneous sarcoidosis lesionsAntimycobacterial therapyLesion diameterCutaneous sarcoidosisSarcoidosis lesionsDisease severityPlacebo-controlled studyPlacebo-treated groupCompletion of therapyT cell functionChronic granulomatous diseaseT cell receptor stimulationSignificant reductionConcomitant levofloxacinPlacebo regimenRifampin regimenSingle-MaskedPlacebo groupTreat analysisDermatology centersTherapeutic optionsGranulomatous diseaseT cellsLesion severity
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 findingsClara 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
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