2020
A Network of Sputum MicroRNAs is Associated with Neutrophilic Airway Inflammation in Asthma
Gomez JL, Chen A, Diaz MP, Zirn N, Gupta A, Britto C, Sauler M, Yan X, Stewart E, Santerian K, Grant N, Liu Q, Fry R, Rager J, Cohn L, Alexis N, Chupp GL. A Network of Sputum MicroRNAs is Associated with Neutrophilic Airway Inflammation in Asthma. American Journal Of Respiratory And Critical Care Medicine 2020, 0: 51-64. PMID: 32255668, PMCID: PMC7328332, DOI: 10.1164/rccm.201912-2360oc.Peer-Reviewed Original ResearchConceptsEndoplasmic reticulum stressAirway inflammationNeutrophil countClinical featuresT-helper cell type 17Neutrophilic airway inflammationReticulum stressSputum of subjectsLung function impairmentHistory of hospitalizationNumber of neutrophilsPeripheral blood neutrophilsSputum of patientsMicroRNA expressionAsthma severityTh17 pathwayFunction impairmentAirway samplesMicroRNA networkBlood neutrophilsOzone exposureAsthmaSputumCellular sourceClinical phenotype
2019
Epigenetics in Asthma
Gomez JL. Epigenetics in Asthma. Current Allergy And Asthma Reports 2019, 19: 56. PMID: 31776749, PMCID: PMC6986424, DOI: 10.1007/s11882-019-0886-y.BooksConceptsChildhood asthmaCommon chronic respiratory diseasePurpose of ReviewAsthmaChronic respiratory diseasesUnderlying pathophysiological processesHuman asthmaAllergic inflammationAsthma endotypesHealthcare utilizationAsthma pathogenesisEpigenetic mechanismsImmune cellsRespiratory diseaseAsthmaHuman studiesPathophysiological processesSummaryThis reviewSpecific methylation signaturesNovel findingsMethylation signaturesCurrent literatureAdditional researchFuture studiesRegulatory roleEndotypes
2016
Noninvasive Analysis of the Sputum Transcriptome Discriminates Clinical Phenotypes of Asthma
Yan X, Chu JH, Gomez J, Koenigs M, Holm C, He X, Perez MF, Zhao H, Mane S, Martinez FD, Ober C, Nicolae DL, Barnes KC, London SJ, Gilliland F, Weiss ST, Raby BA, Cohn L, Chupp GL. Noninvasive Analysis of the Sputum Transcriptome Discriminates Clinical Phenotypes of Asthma. Annals Of The American Thoracic Society 2016, 13 Suppl 1: s104-5. PMID: 27027945, PMCID: PMC5015745, DOI: 10.1513/annalsats.201510-681mg.Peer-Reviewed Original ResearchNitric oxide levelsOxide levelsHigher bronchodilator responseHistory of intubationNormal lung functionClusters of patientsCommon transcriptomic signaturesHigh ratePrebronchodilator FEV1Severe asthmaSteroid requirementsInflammatory characteristicsLung functionBronchodilator responseControl subjectsAsthmaHeterogeneous diseaseClinical phenotypeGene signaturePhysiologic characteristicsWhole bloodTranscriptomic signaturesCluster 1DiseaseHospitalization
2015
Noninvasive Analysis of the Sputum Transcriptome Discriminates Clinical Phenotypes of Asthma
Yan X, Chu JH, Gomez J, Koenigs M, Holm C, He X, Perez MF, Zhao H, Mane S, Martinez FD, Ober C, Nicolae DL, Barnes KC, London SJ, Gilliland F, Weiss ST, Raby BA, Cohn L, Chupp GL. Noninvasive Analysis of the Sputum Transcriptome Discriminates Clinical Phenotypes of Asthma. American Journal Of Respiratory And Critical Care Medicine 2015, 191: 1116-1125. PMID: 25763605, PMCID: PMC4451618, DOI: 10.1164/rccm.201408-1440oc.Peer-Reviewed Original ResearchConceptsHistory of intubationNitric oxide levelsOxide levelsClinical phenotypeMost subjectsHigher bronchodilator responseNormal lung functionBlood of patientsCohort of childrenLogistic regression analysisSputum gene expressionBlood of childrenAirway transcriptomeMilder asthmaPathophysiologic heterogeneityPrebronchodilator FEV1Steroid requirementsLung functionBronchodilator responseGene expressionPhenotype of diseaseAsthmaBlood samplesGene signatureIntubationGenetic variation in chitinase 3-like 1 (CHI3L1) contributes to asthma severity and airway expression of YKL-40
Gomez JL, Crisafi GM, Holm CT, Meyers DA, Hawkins GA, Bleecker ER, Jarjour N, Investigators S, Cohn L, Chupp GL. Genetic variation in chitinase 3-like 1 (CHI3L1) contributes to asthma severity and airway expression of YKL-40. Journal Of Allergy And Clinical Immunology 2015, 136: 51-58.e10. PMID: 25592985, PMCID: PMC4494869, DOI: 10.1016/j.jaci.2014.11.027.Peer-Reviewed Original ResearchConceptsYKL-40 levelsYKL-40 expressionSerum YKL-40 levelsAsthma severityYKL-40Airway expressionAirway diseaseLung functionSingle nucleotide polymorphismsChitinase 3Severe Asthma Research ProgramHigh YKL-40 expressionOnly single nucleotide polymorphismRisk allele APostbronchodilator FEV1Airflow obstructionFEV1 percentSevere asthmaAsthmatic subjectsAsthma prevalenceHaplotype analysisGene polymorphismsG alleleCHI3L1 geneAsthma