2015
Regulation of Retinoic Acid Receptor Beta by Interleukin-15 in the Lung during Cigarette Smoking and Influenza Virus Infection
Wang J, Liu W, Marion C, Singh R, Andrews N, Lee CG, Elias JA, Dela Cruz CS. Regulation of Retinoic Acid Receptor Beta by Interleukin-15 in the Lung during Cigarette Smoking and Influenza Virus Infection. American Journal Of Respiratory Cell And Molecular Biology 2015, 53: 822-833. PMID: 25923039, PMCID: PMC4742936, DOI: 10.1165/rcmb.2014-0448oc.Peer-Reviewed Original ResearchConceptsInfluenza virus infectionCS exposureVirus infectionIL-15WT miceIL-15 knockout miceIL-15 receptor αIL-15 transgenic miceLong-term CS exposureChronic obstructive pulmonary diseaseIL-15tg miceLung interstitial macrophagesCigarette smoke exposureVirus-induced exacerbationsObstructive pulmonary diseaseAntiviral immune responseWild-type miceRetinoic acid receptor betaRA receptor βAcid receptor betaLung injuryLung functionPulmonary diseaseRARβ expressionSmoke exposureMitochondrial Regulation of Inflammasome Activation in Chronic Obstructive Pulmonary Disease
Yoon CM, Nam M, Oh YM, Dela Cruz CS, Kang MJ. Mitochondrial Regulation of Inflammasome Activation in Chronic Obstructive Pulmonary Disease. Journal Of Innate Immunity 2015, 8: 121-128. PMID: 26536345, PMCID: PMC4801739, DOI: 10.1159/000441299.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseObstructive pulmonary diseaseCigarette smokeInflammasome activationPulmonary diseaseInflammatory responsePathogenesis of COPDMajor unmet medical needLung inflammatory responseUnmet medical needInnate immune signalingChronic airwayImmune driversPulmonary inflammationCOPD pathogenesisNoxious particlesMedical needImmune signalingInflammationPathogenesisDiseaseActivationCentral playerResponseAirway
2010
Role of Breast Regression Protein–39 in the Pathogenesis of Cigarette Smoke–Induced Inflammation and Emphysema
Matsuura H, Hartl D, Kang MJ, Dela Cruz CS, Koller B, Chupp GL, Homer RJ, Zhou Y, Cho WK, Elias JA, Lee CG. Role of Breast Regression Protein–39 in the Pathogenesis of Cigarette Smoke–Induced Inflammation and Emphysema. American Journal Of Respiratory Cell And Molecular Biology 2010, 44: 777-786. PMID: 20656949, PMCID: PMC3135840, DOI: 10.1165/rcmb.2010-0081oc.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseBRP-39/YKLBreast regression protein 39YKL-40BRP-39Alveolar destructionCigarette smokeChitinase-like protein YKL-40Emphysematous alveolar destructionLungs of CSObstructive pulmonary diseaseProtein YKL-40Excessive inflammatory responseAirway epithelial cellsAlveolar type II cellsNull mutant miceProtein 39Epithelial cell apoptosisType II cellsCurrent smokersPulmonary diseaseBronchoalveolar lavageTissue inflammationEmphysematous destructionSerum concentrations