2022
Epidermal Growth Factor Receptor Inhibition Is Protective in Hyperoxia‐Induced Lung Injury
Harris ZM, Sun Y, Joerns J, Clark B, Hu B, Korde A, Sharma L, Shin HJ, Manning EP, Placek L, Unutmaz D, Stanley G, Chun H, Sauler M, Rajagopalan G, Zhang X, Kang MJ, Koff JL. Epidermal Growth Factor Receptor Inhibition Is Protective in Hyperoxia‐Induced Lung Injury. Oxidative Medicine And Cellular Longevity 2022, 2022: 9518592. PMID: 36193076, PMCID: PMC9526641, DOI: 10.1155/2022/9518592.Peer-Reviewed Original ResearchConceptsAcute lung injuryEpidermal growth factor receptorAlveolar epithelial cellsLung injurySevere hyperoxiaEGFR inhibitionEpithelial cellsHyperoxia-Induced Lung InjuryRole of EGFRMurine alveolar epithelial cellsGrowth factor receptor inhibitionWorse clinical outcomesEpidermal growth factor receptor inhibitionHuman alveolar epithelial cellsWild-type littermatesPoly (ADP-ribose) polymeraseTerminal dUTP nickGrowth factor receptorClinical outcomesImproved survivalReceptor inhibitionLung repairProtective roleComplex roleEGFR deletion
2018
Respiratory syncytial virus activates epidermal growth factor receptor to suppress interferon regulatory factor 1-dependent interferon-lambda and antiviral defense in airway epithelium
Kalinowski A, Galen B, Ueki I, Sun Y, Mulenos A, Osafo-Addo A, Clark B, Joerns J, Liu W, Nadel J, Dela Cruz C, Koff J. Respiratory syncytial virus activates epidermal growth factor receptor to suppress interferon regulatory factor 1-dependent interferon-lambda and antiviral defense in airway epithelium. Mucosal Immunology 2018, 11: 958-967. PMID: 29411775, PMCID: PMC6431552, DOI: 10.1038/mi.2017.120.Peer-Reviewed Original ResearchConceptsRespiratory syncytial virusEpidermal growth factor receptorEGFR inhibitionGrowth factor receptorRSV infectionSyncytial virusViral infectionRegulatory factor 1Lower respiratory tract infectionsIFN-λ productionRespiratory tract infectionsChronic lung diseaseFactor receptorAntiviral immune responseFactor 1RSV F proteinType III IFNsAntiviral defenseEGFR activationInnate antiviral responseInterferon regulatory factor 1Cause pneumoniaRSV inducesSignificant IFNTyrosine kinase receptors
2014
EGFR activation suppresses respiratory virus-induced IRF1-dependent CXCL10 production
Kalinowski A, Ueki I, Min-Oo G, Ballon-Landa E, Knoff D, Galen B, Lanier LL, Nadel JA, Koff JL. EGFR activation suppresses respiratory virus-induced IRF1-dependent CXCL10 production. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2014, 307: l186-l196. PMID: 24838750, PMCID: PMC4101792, DOI: 10.1152/ajplung.00368.2013.Peer-Reviewed Original ResearchConceptsRespiratory viral infectionsRespiratory syncytial virusCXCL10 productionRespiratory virusesViral infectionIFN regulatory factorAirway epitheliumEGFR activationChronic obstructive pulmonary diseaseEpithelial cellsExacerbation of asthmaObstructive pulmonary diseaseRecruitment of lymphocytesAdaptive immune responsesAirway epithelial cellsNADPH oxidase activationInhibition of EGFRVirus-infected cellsHuman viral pathogensPulmonary diseaseSyncytial virusEpithelial productionIL-8Viral pneumoniaEpidermal growth factor receptor (EGFR) activation
2013
Respiratory virus–induced EGFR activation suppresses IRF1-dependent interferon λ and antiviral defense in airway epithelium
Ueki IF, Min-Oo G, Kalinowski A, Ballon-Landa E, Lanier LL, Nadel JA, Koff JL. Respiratory virus–induced EGFR activation suppresses IRF1-dependent interferon λ and antiviral defense in airway epithelium. Journal Of Experimental Medicine 2013, 210: 1929-1936. PMID: 23999497, PMCID: PMC3782052, DOI: 10.1084/jem.20121401.Peer-Reviewed Original ResearchConceptsEpithelial epidermal growth factor receptorViral infectionHost responseInnate antiviral host responsesEGFR activationIFN-λ productionIFN-λ signalingAntiviral immune responseImportance of IFNType III IFNsAntiviral defenseAntiviral host responseEpidermal growth factor receptorGrowth factor receptorSignificant IFNTyrosine kinase receptorsInterferon λNovel therapiesAirway epitheliumIFN regulatory factor-1Immune responseFuture therapiesViral pathogenesisAntiviral responseIFN
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
2007
Regulation of interleukin-8 via an airway epithelial signaling cascade
Nakanaga T, Nadel JA, Ueki IF, Koff JL, Shao MX. Regulation of interleukin-8 via an airway epithelial signaling cascade. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2007, 292: l1289-l1296. PMID: 17220369, DOI: 10.1152/ajplung.00356.2006.Peer-Reviewed Original ResearchConceptsIL-8 productionIL-8 expressionHuman airway epithelial NCI-H292 cellsEGF receptorNeutrophil chemoattractant interleukinEpithelial cellsNCI-H292 cellsAirway epithelial cellsModel inflammatory stimulusNegative bacterial lipopolysaccharideDual oxidase 1MAP kinases ERK1/2IL-8Tumor necrosisInterleukin-8Immune organsInflammatory stimuliMucin productionHuman airwaysAirwayEpithelial defenseTACE activationBacterial infectionsHost defenseConverting enzyme
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 1