2025
Proinflammatory Pulmonary Effects of SARS-CoV-2 Main Protease in Mice and Human Bronchial Epithelial Cells
Caceres A, Jabba S, Jordt S. Proinflammatory Pulmonary Effects of SARS-CoV-2 Main Protease in Mice and Human Bronchial Epithelial Cells. American Journal Of Respiratory And Critical Care Medicine 2025, 211: a6597-a6597. DOI: 10.1164/ajrccm.2025.211.abstracts.a6597.Peer-Reviewed Original ResearchHuman bronchial epithelial cellsSARS-CoV-2 main proteaseBronchial epithelial cellsEpithelial cellsMain protease
2024
Next generation triplex-forming PNAs for site-specific genome editing of the F508del CFTR mutation
Gupta A, Barone C, Quijano E, Piotrowski-Daspit A, Perera J, Riccardi A, Jamali H, Turchick A, Zao W, Saltzman W, Glazer P, Egan M. Next generation triplex-forming PNAs for site-specific genome editing of the F508del CFTR mutation. Journal Of Cystic Fibrosis 2024, 24: 142-148. PMID: 39107154, PMCID: PMC11788067, DOI: 10.1016/j.jcf.2024.07.009.Peer-Reviewed Original ResearchCystic fibrosis transmembrane conductance regulatorCystic fibrosis transmembrane conductance regulator geneF508del-CFTR mutationPeptide nucleic acidCFBE cellsBronchial epithelial cellsCystic fibrosisTriplex-forming peptide nucleic acidsDonor DNACFTR mutationsEpithelial cellsCFTR functionMutations associated with genetic diseasesPrimary nasal epithelial cellsAnalysis of genomic DNAGenetic diseasesIncreased CFTR functionDevelopment of peptide nucleic acidsImprove CFTR functionTransmembrane conductance regulatorAutosomal recessive genetic diseaseNasal epithelial cellsAir-liquid interfaceCystic fibrosis bronchial epithelial cellsHuman bronchial epithelial cellsSARS-CoV-2-related bat viruses evade human intrinsic immunity but lack efficient transmission capacity
Peña-Hernández M, Alfajaro M, Filler R, Moriyama M, Keeler E, Ranglin Z, Kong Y, Mao T, Menasche B, Mankowski M, Zhao Z, Vogels C, Hahn A, Kalinich C, Zhang S, Huston N, Wan H, Araujo-Tavares R, Lindenbach B, Homer R, Pyle A, Martinez D, Grubaugh N, Israelow B, Iwasaki A, Wilen C. SARS-CoV-2-related bat viruses evade human intrinsic immunity but lack efficient transmission capacity. Nature Microbiology 2024, 9: 2038-2050. PMID: 39075235, DOI: 10.1038/s41564-024-01765-z.Peer-Reviewed Original ResearchBat coronavirusesRelatives of SARS-CoV-2Upper airwayUpper airways of miceEpithelial cellsHuman nasal epithelial cellsAirways of miceMajor histocompatibility complex class I.SARS-CoV-2Nasal epithelial cellsHistocompatibility complex class I.Human bronchial epithelial cellsGenetic similarityBronchial epithelial cellsInnate immune restrictionCoronavirus replicationFunctional characterizationMolecular cloningReduced pathogenesisImpaired replicationBat virusCoronavirus pathogenesisPandemic potentialHigh-risk familiesImmune restriction
2022
Bronchial epithelium epithelial-mesenchymal plasticity forms aberrant basaloid-like cells in vitro
Uthaya Kumar DB, Motakis E, Yurieva M, Kohar V, Martinek J, Wu TC, Khoury J, Grassmann J, Lu M, Palucka K, Kaminski N, Koff JL, Williams A. Bronchial epithelium epithelial-mesenchymal plasticity forms aberrant basaloid-like cells in vitro. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2022, 322: l822-l841. PMID: 35438006, PMCID: PMC9142163, DOI: 10.1152/ajplung.00254.2021.Peer-Reviewed Original ResearchConceptsProtein codingEpithelial-mesenchymal transitionLncRNA genesEMT inductionSingle-cell RNA sequencingSingle-cell RNA-seq dataEpithelial-mesenchymal plasticityRNA-seq dataMechanisms of EMTSingle-cell levelEpithelial cell typesRole of EMTTranscriptional reprogrammingHuman bronchial epithelial cellsRNA genesEMT gene signatureTranscriptional changesTranscriptional differencesRNA sequencingSpecific lncRNAsBronchial epithelial cellsDifferential expressionMyofibroblast conversionCell typesGenesSurface conjugation of antibodies improves nanoparticle uptake in bronchial epithelial cells
Luks VL, Mandl H, DiRito J, Barone C, Freedman-Weiss MR, Ricciardi AS, Tietjen GG, Egan ME, Saltzman WM, Stitelman DH. Surface conjugation of antibodies improves nanoparticle uptake in bronchial epithelial cells. PLOS ONE 2022, 17: e0266218. PMID: 35385514, PMCID: PMC8986008, DOI: 10.1371/journal.pone.0266218.Peer-Reviewed Original ResearchConceptsTarget-specific antibodiesNanoparticle uptakeSurface conjugationNanoparticle surface modificationSurface of nanoparticlesCellular uptakeSite-specific geneSpecific cellular bindingNanoparticlesIntracellular deliveryEditing reagentsBronchial epithelial cellsSurface modificationCellular targetingCystic fibrosisTherapeutic agentsEpithelial cellsParticle uptakeFeasible strategyGenetic diseasesFirst demonstrationHuman bronchial epithelial cellsKinetics of antibodiesCellular bindingAppropriate antibodies
2021
Single-cell longitudinal analysis of SARS-CoV-2 infection in human airway epithelium identifies target cells, alterations in gene expression, and cell state changes
Ravindra NG, Alfajaro MM, Gasque V, Huston NC, Wan H, Szigeti-Buck K, Yasumoto Y, Greaney AM, Habet V, Chow RD, Chen JS, Wei J, Filler RB, Wang B, Wang G, Niklason LE, Montgomery RR, Eisenbarth SC, Chen S, Williams A, Iwasaki A, Horvath TL, Foxman EF, Pierce RW, Pyle AM, van Dijk D, Wilen CB. Single-cell longitudinal analysis of SARS-CoV-2 infection in human airway epithelium identifies target cells, alterations in gene expression, and cell state changes. PLOS Biology 2021, 19: e3001143. PMID: 33730024, PMCID: PMC8007021, DOI: 10.1371/journal.pbio.3001143.Peer-Reviewed Original ResearchConceptsSARS-CoV-2 infectionSARS-CoV-2Human bronchial epithelial cellsInterferon-stimulated genesCell state changesAcute respiratory syndrome coronavirus 2 infectionSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infectionSyndrome coronavirus 2 infectionCell tropismCoronavirus 2 infectionCoronavirus disease 2019Onset of infectionCell-intrinsic expressionCourse of infectionAir-liquid interface culturesHost-viral interactionsBronchial epithelial cellsSingle-cell RNA sequencingCell typesIL-1Disease 2019Human airwaysDevelopment of therapeuticsDrug AdministrationViral replicationGenetic variants are identified to increase risk of COVID-19 related mortality from UK Biobank data
Hu J, Li C, Wang S, Li T, Zhang H. Genetic variants are identified to increase risk of COVID-19 related mortality from UK Biobank data. Human Genomics 2021, 15: 10. PMID: 33536081, PMCID: PMC7856608, DOI: 10.1186/s40246-021-00306-7.Peer-Reviewed Original ResearchConceptsGenome-wide association studiesGenetic variantsPower of GWASTraditional genome-wide association studiesTraits of interestMulti-locus interactionsHuman bronchial epithelial cellsSignificant genetic variantsDownregulated genesChromosome 2Genetic basisGenetic factorsAssociation studiesBronchial epithelial cellsCilia dysfunctionSusceptibility lociMitochondrial dysfunctionGenome-wide significant genetic variantsEpithelial cellsGenesMolecular pathogenesisHost genetic factorsUK Biobank dataUK BiobankVariantsLong noncoding RNA TINCR is a novel regulator of human bronchial epithelial cell differentiation state
Omote N, Sakamoto K, Li Q, Schupp JC, Adams T, Ahangari F, Chioccioli M, DeIuliis G, Hashimoto N, Hasegawa Y, Kaminski N. Long noncoding RNA TINCR is a novel regulator of human bronchial epithelial cell differentiation state. Physiological Reports 2021, 9: e14727. PMID: 33527707, PMCID: PMC7851438, DOI: 10.14814/phy2.14727.Peer-Reviewed Original ResearchConceptsTerminal differentiation-induced lncRNANormal human bronchial epithelial cellsTINCR overexpressionCell differentiationNotch genesTissue developmentBronchial epithelial cellsExtracellular matrix organizationCell phenotypeRNA sequencing analysisNumerous biological functionsRole of lncRNAsCell differentiation stateEpithelial cellsHuman bronchial epithelial cellsCiliated cell differentiationStaufen1 proteinNovel regulatorBasal cell phenotypeDownstream regulatorsRNA immunoprecipitationBiological functionsCritical regulatorDifferential expressionDifferentiation state
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
2018
A transcription factor network represses CFTR gene expression in airway epithelial cells.
Mutolo MJ, Leir SH, Fossum SL, Browne JA, Harris A. A transcription factor network represses CFTR gene expression in airway epithelial cells. Biochemical Journal 2018, 475: 1323-1334. PMID: 29572268, PMCID: PMC6380350, DOI: 10.1042/bcj20180044.Peer-Reviewed Original ResearchConceptsCystic fibrosisTranscription factorsAirway epitheliumEpithelial cellsCalu-3 lung epithelial cellsPrimary human bronchial epithelial cellsAirway epithelium resultsKrüppel-like factor 5Novel therapeutic targetAirway epithelial cellsEts homologous factorHuman bronchial epithelial cellsTranscription factor networkBronchial epithelial cellsLung epithelial cellsTissue-specific enhancersCystic fibrosis transmembrane conductance regulator (CFTR) geneCFTR gene expressionAirway expressionTransmembrane conductance regulator geneLung diseaseCFTR mRNA levelsPancreatic ductTherapeutic targetCF morbidity
2016
Airway Secretory microRNAome Changes during Rhinovirus Infection in Early Childhood
Gutierrez M, Gomez J, Perez G, Pancham K, Val S, Pillai D, Giri M, Ferrante S, Freishtat R, Rose M, Preciado D, Nino G. Airway Secretory microRNAome Changes during Rhinovirus Infection in Early Childhood. PLOS ONE 2016, 11: e0162244. PMID: 27643599, PMCID: PMC5028059, DOI: 10.1371/journal.pone.0162244.Peer-Reviewed Original ResearchConceptsRV infectionHuman bronchial epithelial cellsAirway secretionsExtracellular vesiclesCause of asthma exacerbationsAirways of young childrenHuman RV infectionsNasal airway secretionsHsa-miR-155Air-liquid interfaceRegulates antiviral immunityMonitor respiratory conditionsSecretion of extracellular vesiclesModify gene expressionAirways of individualsPotential biological relevanceBronchial epithelial cellsAge-matched controlsInnate immune responseDevelopment of asthmaBioinformatics toolsGene datasetsGenetic communicationNoncoding RNA moleculesRNA moleculesTwo interferon-independent double-stranded RNA-induced host defense strategies suppress the common cold virus at warm temperature
Foxman EF, Storer JA, Vanaja K, Levchenko A, Iwasaki A. Two interferon-independent double-stranded RNA-induced host defense strategies suppress the common cold virus at warm temperature. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: 8496-8501. PMID: 27402752, PMCID: PMC4968739, DOI: 10.1073/pnas.1601942113.Peer-Reviewed Original ResearchConceptsIFN-independent mechanismsEpithelial cellsHost defense strategiesHost cell deathIFN inductionHuman bronchial epithelial cellsReduced virus productionCommon cold virusInfected epithelial cellsB-cell lymphoma 2 (Bcl-2) overexpressionBronchial epithelial cellsDiverse stimuliViral replicationAntiviral pathwaysCell deathH1-HeLa cellsTemperature-dependent replicationCell typesSingle replication cycleTemperature-dependent growthReplication cycleWarmer temperaturesCool temperaturesDefense strategiesType 1 IFN response
2015
Baseline Chromatin Modification Levels May Predict Interindividual Variability in Ozone-Induced Gene Expression
McCullough S, Bowers E, On D, Morgan D, Dailey L, Hines R, Devlin R, Diaz-Sanchez D. Baseline Chromatin Modification Levels May Predict Interindividual Variability in Ozone-Induced Gene Expression. Toxicological Sciences 2015, 150: 216-224. PMID: 26719369, PMCID: PMC4838038, DOI: 10.1093/toxsci/kfv324.Peer-Reviewed Original ResearchConceptsChromatin modificationsH3 lysine 4 trimethylationSpecific chromatin modificationsChromatin modification statesLysine 4 trimethylationUnmodified H3Human bronchial epithelial cellsModification statesTotal H3H3K27 acetylationCellular signalsGene inductionPrimary human bronchial epithelial cellsKey regulatorGene expressionEpigenetic markersBronchial epithelial cellsTraditional toxicological paradigmModification levelsRelative abundanceAir-liquid interface modelTrimethylationEpithelial cellsH3Specific modifications
2014
An Optimized Protocol for Isolating Primary Epithelial Cell Chromatin for ChIP
Browne JA, Harris A, Leir SH. An Optimized Protocol for Isolating Primary Epithelial Cell Chromatin for ChIP. PLOS ONE 2014, 9: e100099. PMID: 24971909, PMCID: PMC4074041, DOI: 10.1371/journal.pone.0100099.Peer-Reviewed Original ResearchConceptsCell typesChromatin immunoprecipitation dataDNA-binding proteinsLysis bufferPrimary human epithelial cellsEpithelial cell typesEpithelial cellsChromatin purificationHuman bronchial epithelial cellsENCODE consortiumHuman epithelial cellsCell chromatinNext-generation sequencingImmunoprecipitation dataCell lysis procedurePrimary human bronchial epithelial cellsChromatinFormaldehyde-fixed cellsBronchial epithelial cellsMembrane lysisSize selectionLysis procedureAdherent cellsCellsLysis step
2013
Aldehyde dehydrogenase 3A1 protects airway epithelial cells from cigarette smoke-induced DNA damage and cytotoxicity
Jang JH, Bruse S, Liu Y, Duffy V, Zhang C, Oyamada N, Randell S, Matsumoto A, Thompson DC, Lin Y, Vasiliou V, Tesfaigzi Y, Nyunoya T. Aldehyde dehydrogenase 3A1 protects airway epithelial cells from cigarette smoke-induced DNA damage and cytotoxicity. Free Radical Biology And Medicine 2013, 68: 80-86. PMID: 24316006, PMCID: PMC3941192, DOI: 10.1016/j.freeradbiomed.2013.11.028.Peer-Reviewed Original ResearchConceptsHuman bronchial epithelial cellsImmortalized human bronchial epithelial cellsCigarette smokeALDH enzymatic activityCigarette smoke-induced DNA damageAldehyde dehydrogenase 3A1Smoke-induced DNA damagePrimary human bronchial epithelial cellsEpithelial cellsCSE-exposed cellsCSE-induced cytotoxicityBronchial epithelial cellsDNA damageExtract exposureMRNA levelsEffects of overexpression
2012
Effect of KRAS Oncogene Substitutions on Protein Behavior: Implications for Signaling and Clinical Outcome
Ihle NT, Byers LA, Kim ES, Saintigny P, Lee JJ, Blumenschein GR, Tsao A, Liu S, Larsen JE, Wang J, Diao L, Coombes KR, Chen L, Zhang S, Abdelmelek MF, Tang X, Papadimitrakopoulou V, Minna JD, Lippman SM, Hong WK, Herbst RS, Wistuba II, Heymach JV, Powis G. Effect of KRAS Oncogene Substitutions on Protein Behavior: Implications for Signaling and Clinical Outcome. Journal Of The National Cancer Institute 2012, 104: 228-239. PMID: 22247021, PMCID: PMC3274509, DOI: 10.1093/jnci/djr523.Peer-Reviewed Original ResearchMeSH KeywordsAspartic AcidCarcinoma, Non-Small-Cell LungCell Line, TumorClinical Trials, Phase II as TopicCysteineDisease-Free SurvivalGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, rasGenetic VectorsGlycineHumansImmunoblottingImmunoprecipitationKaplan-Meier EstimateLentivirusLung NeoplasmsMicroarray AnalysisMolecular Targeted TherapyMutationProto-Oncogene Proteins c-aktRandomized Controlled Trials as TopicSignal TransductionTOR Serine-Threonine KinasesTreatment OutcomeValineConceptsNon-small cell lung cancerKirsten rat sarcoma viral oncogene homologProgression-free survivalNSCLC cell linesWild-type KRASMutant KRASRefractory non-small cell lung cancerWorse progression-free survivalRat sarcoma viral oncogene homologRas2 Kirsten rat sarcoma viral oncogene homologSarcoma viral oncogene homologKaplan-Meier curvesCell lung cancerReverse-phase protein array studiesKRas proteinsHuman bronchial epithelial cellsCancer cell growthPatient tumor samplesCell linesImmortalized human bronchial epithelial cellsBronchial epithelial cellsProtein array studiesTumor gene expressionEvaluable patientsClinical outcomes
2009
Role of Double-Stranded RNA Pattern Recognition Receptors in Rhinovirus-Induced Airway Epithelial Cell Responses
Wang Q, Nagarkar DR, Bowman ER, Schneider D, Gosangi B, Lei J, Zhao Y, McHenry CL, Burgens RV, Miller DJ, Sajjan U, Hershenson MB. Role of Double-Stranded RNA Pattern Recognition Receptors in Rhinovirus-Induced Airway Epithelial Cell Responses. The Journal Of Immunology 2009, 183: 6989-6997. PMID: 19890046, PMCID: PMC2920602, DOI: 10.4049/jimmunol.0901386.Peer-Reviewed Original ResearchMeSH KeywordsBlotting, WesternCell LineDEAD Box Protein 58DEAD-box RNA HelicasesEpithelial CellsGene ExpressionHumansInterferon-Induced Helicase, IFIH1Picornaviridae InfectionsReceptors, ImmunologicReceptors, Pattern RecognitionRespiratory MucosaReverse Transcriptase Polymerase Chain ReactionRhinovirusRNA, Double-StrandedRNA, Small InterferingSignal TransductionToll-Like Receptor 3ConceptsIL-8/CXCL8RV-1BChronic obstructive pulmonary disease exacerbationsObstructive pulmonary disease exacerbationsGM-CSFMelanoma differentiation-associated geneAirway epithelial cell responsesIFN-lambda1Pulmonary disease exacerbationsBEAS-2B human bronchial epithelial cellsRetinoic acid-inducible geneToll/IL-1RHuman bronchial epithelial cellsPattern recognition receptorsEpithelial cell responsesUV-irradiated virusBronchial epithelial cellsAcid-inducible geneBEAS-2B cellsDisease exacerbationTLR-3IFN response factorsCommon coldIL-1RIFN expression
2008
Multiple TLRs activate EGFR via a signaling cascade to produce innate immune responses in airway epithelium
Koff JL, Shao MX, Ueki IF, Nadel JA. Multiple TLRs activate EGFR via a signaling cascade to produce innate immune responses in airway epithelium. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2008, 294: l1068-l1075. PMID: 18375743, DOI: 10.1152/ajplung.00025.2008.Peer-Reviewed Original ResearchMeSH KeywordsADAM ProteinsADAM17 ProteinBronchiCells, CulturedDual OxidasesErbB ReceptorsHumansImmunity, InnateInterleukin-8NADPH OxidasesReactive Oxygen SpeciesRespiratory MucosaRNA, Small InterferingSignal TransductionToll-Like ReceptorsTransforming Growth Factor alphaVascular Endothelial Growth Factor AConceptsToll-like receptorsTNF-alpha converting enzymeInnate immune responseMultiple Toll-like receptorsIL-8Immune responseTGF-alphaVEGF productionTLR ligandsAirway epitheliumEpithelial cellsCertain innate immune responsesEGF receptorMultiple TLR ligandsAirway epithelial surfaceAirway epithelial cell lineNormal human bronchial epithelial cellsEpithelial cell productionAirway epithelial cellsHuman bronchial epithelial cellsNADPH oxidase inhibitorBronchial epithelial cellsEpithelial cell lineReactive oxygen species (ROS) scavengerEpithelial production
2006
Pseudomonas Lipopolysaccharide Accelerates Wound Repair via Activation of a Novel Epithelial Cell Signaling Cascade
Koff JL, Shao MX, Kim S, Ueki IF, Nadel JA. Pseudomonas Lipopolysaccharide Accelerates Wound Repair via Activation of a Novel Epithelial Cell Signaling Cascade. The Journal Of Immunology 2006, 177: 8693-8700. PMID: 17142770, DOI: 10.4049/jimmunol.177.12.8693.Peer-Reviewed Original ResearchConceptsTNF-alpha converting enzymeEGFR phosphorylationOxidase 1Wound repairNCI-H292 human airway epithelial cellsEpidermal growth factor receptor (EGFR) activationGrowth factor receptor activationAirway epithelial cellsEpithelial cellsCell signaling cascadesNormal human bronchial epithelial cellsTLR-4Airway epitheliumHuman bronchial epithelial cellsReactive oxygen species (ROS) scavengerPhosphorylation pathwaySignaling cascadesEssential functionsBronchial epithelial cellsEGFR ligandsHuman airway epithelial cellsChronic airway diseasesOxygen species scavengersPseudomonas bacteriaDual oxidase 1Smoking is associated with increased telomerase activity in short-term cultures of human bronchial epithelial cells
Yim HW, Slebos RJ, Randell SH, Umbach DM, Parsons AM, Rivera MP, Detterbeck FC, Taylor JA. Smoking is associated with increased telomerase activity in short-term cultures of human bronchial epithelial cells. Cancer Letters 2006, 246: 24-33. PMID: 16517060, DOI: 10.1016/j.canlet.2006.01.023.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAged, 80 and overBronchiCell Culture TechniquesCell ProliferationCells, CulturedCellular SenescenceChildDNA MethylationEpithelial CellsFemaleHumansLung NeoplasmsMaleMiddle AgedPolymerase Chain ReactionPromoter Regions, GeneticSmokingTelomeraseTime FactorsTumor Cells, CulturedConceptsNormal bronchial epitheliumTelomeric repeat amplification protocolHuman bronchial epithelial cellsBronchial epithelial cellsBronchial epitheliumTelomerase activityLung cancer historyLung cancer statusEpithelial cellsMaximum passage numberTobacco carcinogen exposureHBE cell culturesRepeat amplification protocolExtended culturingHTERT promoterShort-term cultureSmoking historyTobacco smokingPassage numberCancer historyLung carcinogenesisLung carcinomaCancer statusCarcinogen exposureCausative role
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