2022
CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging.
Cui H, Xie N, Banerjee S, Dey T, Liu RM, Antony VB, Sanders YY, Adams TS, Gomez JL, Thannickal VJ, Kaminski N, Liu G. CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging. American Journal Of Respiratory And Critical Care Medicine 2022, 206: 459-475. PMID: 35687485, DOI: 10.1164/rccm.202109-2151oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisLung fibrosisCD38 expressionAlveolar epithelial cell injuryEpithelial cell injuryEffective therapeutic strategyHuman lung parenchymaIPF lungsLung functionPulmonary fibrosisDisease progressionFibrotic lungsReal-time PCRYoung miceLung parenchymaOld miceCell injuryTherapeutic strategiesFibrosisPharmacological inactivationCD38Single-cell RNA sequencingFlow cytometryWestern blottingOld animals
2021
Inhibition of PDIA3 in club cells attenuates osteopontin production and lung fibrosis
Kumar A, Elko E, Bruno SR, Mark ZF, Chamberlain N, Mihavics BK, Chandrasekaran R, Walzer J, Ruban M, Gold C, Lam YW, Ghandikota S, Jegga AG, Gomez JL, Janssen-Heininger YM, Anathy V. Inhibition of PDIA3 in club cells attenuates osteopontin production and lung fibrosis. Thorax 2021, 77: 669-678. PMID: 34400514, PMCID: PMC8847543, DOI: 10.1136/thoraxjnl-2021-216882.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisProtein disulfide isomerase A3Lung fibrosisPulmonary fibrosisClub cellsFibrosis-related proteinsMechanism of actionControl patientsLung functionBleomycin modelLung parenchymaFibrosisTherapeutic potentialMiceOsteopontin productionSpecific deletionPatientsProtein signaturesInhibitionResearch ConsortiumPathologyCellsSPP1Human transcriptome datasetsMajor interactorsSPLUNC1: a novel marker of cystic fibrosis exacerbations
Khanal S, Webster M, Niu N, Zielonka J, Nunez M, Chupp G, Slade MD, Cohn L, Sauler M, Gomez JL, Tarran R, Sharma L, Dela Cruz CS, Egan M, Laguna T, Britto CJ. SPLUNC1: a novel marker of cystic fibrosis exacerbations. European Respiratory Journal 2021, 58: 2000507. PMID: 33958427, PMCID: PMC8571118, DOI: 10.1183/13993003.00507-2020.Peer-Reviewed Original ResearchConceptsAcute pulmonary exacerbationsSPLUNC1 levelsCystic fibrosisClinical outcomesCF participantsLong-term disease controlNasal epithelium clone 1Cystic fibrosis exacerbationsHigher AE riskLung function declineCytokines interleukin-1βTumor necrosis factorAE riskClinical worseningPulmonary exacerbationsStable patientsLung functionAirway clearanceFunction declineSputum collectionAcute inflammationInflammatory cytokinesMicrobiology findingsCF careClinical management
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