2018
Impaired type I interferon regulation in the blood transcriptome of recurrent asthma exacerbations
Gomez JL, Diaz MP, Nino G, Britto CJ. Impaired type I interferon regulation in the blood transcriptome of recurrent asthma exacerbations. BMC Medical Genomics 2018, 11: 21. PMID: 29486764, PMCID: PMC5830339, DOI: 10.1186/s12920-018-0340-3.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAsthmaChildFemaleGene Expression RegulationHumansInterferon Type ILeukocytes, MononuclearMaleRecurrenceRhinovirusSTAT1 Transcription FactorTranscriptomeConceptsPeripheral blood mononuclear cellsAsthma exacerbationsInterferon-stimulated genesRespiratory infectionsIL-15Vivo cohortToll-like receptor 2STAT1 responseRecurrent asthma exacerbationsAcute asthma exacerbationPro-inflammatory moleculesType I interferon regulationBlood mononuclear cellsPro-inflammatory signatureTranscriptomic signaturesType I interferonFold changeAdult asthmaAcute phaseMononuclear cellsImmunologic genesExacerbationIndependent cohortReceptor 2I interferon
2015
Bactericidal/Permeability-Increasing Protein Fold–Containing Family Member A1 in Airway Host Protection and Respiratory Disease
Britto CJ, Cohn L. Bactericidal/Permeability-Increasing Protein Fold–Containing Family Member A1 in Airway Host Protection and Respiratory Disease. American Journal Of Respiratory Cell And Molecular Biology 2015, 52: 525-534. PMID: 25265466, PMCID: PMC4491141, DOI: 10.1165/rcmb.2014-0297rt.BooksMeSH KeywordsAnimalsGene Expression RegulationGlycoproteinsHost-Pathogen InteractionsHumansImmunity, InnateInflammation MediatorsLung DiseasesPhosphoproteinsRespiratory MucosaSignal TransductionConceptsPulmonary diseaseHost protectionChronic obstructive pulmonary diseaseObstructive pulmonary diseaseIdiopathic pulmonary fibrosisMember A1Immune cell functionMultiple lung diseasesBactericidal/permeability-increasing proteinRespiratory malignanciesPulmonary pathogenesisPulmonary fibrosisPermeability-increasing proteinRespiratory secretionsLung diseaseUpper airwayRespiratory tractRespiratory diseaseProximal tracheaImmunomodulatory propertiesBPIFA1Cystic fibrosisDiseasePotential drug targetsEnvironmental exposures
2013
Short Palate, Lung, and Nasal Epithelial Clone–1 Is a Tightly Regulated Airway Sensor in Innate and Adaptive Immunity
Britto CJ, Liu Q, Curran DR, Patham B, Dela Cruz CS, Cohn L. Short Palate, Lung, and Nasal Epithelial Clone–1 Is a Tightly Regulated Airway Sensor in Innate and Adaptive Immunity. American Journal Of Respiratory Cell And Molecular Biology 2013, 48: 717-724. PMID: 23470624, PMCID: PMC3727874, DOI: 10.1165/rcmb.2012-0072oc.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAnimalsCell Line, TumorGene Expression RegulationGlycoproteinsHumansImmunity, InnateImmunohistochemistryInflammationInfluenza A virusInterferon-gammaLipopolysaccharidesLungMiceMice, Inbred C57BLPhosphoproteinsPneumonia, BacterialPseudomonas aeruginosaRespiratory MucosaRespiratory Tract InfectionsStreptococcus pneumoniaeConceptsNasal epithelial clone 1Lower respiratory tractRespiratory tractAirway inflammationShort palateTh2-induced airway inflammationHost defenseAllergic airway inflammationCommon respiratory pathogensAirway epithelial cellsModel of pneumoniaAirway surface liquidPathogen-associated molecular patternsGreatest environmental exposureClone 1Mucociliary clearanceRespiratory pathogensAirway sensorsRespiratory epitheliumAdaptive immunitySPLUNC1IFN-γ actBasal conditionsMRNA expressionMolecular patterns