2006
Role of 5-Lipoxygenase in IL-13-Induced Pulmonary Inflammation and Remodeling
Shim YM, Zhu Z, Zheng T, Lee CG, Homer RJ, Ma B, Elias JA. Role of 5-Lipoxygenase in IL-13-Induced Pulmonary Inflammation and Remodeling. The Journal Of Immunology 2006, 177: 1918-1924. PMID: 16849505, DOI: 10.4049/jimmunol.177.3.1918.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArachidonate 5-LipoxygenaseChronic DiseaseDinoprostoneInflammationInterleukin-13LeukotrienesLungMatrix Metalloproteinase 12MetalloendopeptidasesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicPulmonary AlveoliPulmonary FibrosisSignal TransductionTransforming Growth Factor betaTransforming Growth Factor beta1ConceptsIL-13-induced inflammationIL-13Transgenic IL-13Activation of TGFMatrix metalloproteinase-12Th2 inflammationPulmonary inflammationC57BL/6 miceChronic inflammationCysteinyl LTsFibrotic responseLevels of mRNATissue fibrosisLT metabolismInflammationAlveolar remodelingReceptor 1Metalloproteinase-12Pathway activationExaggerated levelsOptimal stimulationCytosolic phospholipasePathogenesisActivation pathwayRemodelingEssential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung
Bhandari V, Choo-Wing R, Chapoval SP, Lee CG, Tang C, Kim YK, Ma B, Baluk P, Lin MI, McDonald DM, Homer RJ, Sessa WC, Elias JA. Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung. Proceedings Of The National Academy Of Sciences Of The United States Of America 2006, 103: 11021-11026. PMID: 16832062, PMCID: PMC1544167, DOI: 10.1073/pnas.0601057103.Peer-Reviewed Original ResearchConceptsInducible NOSNitric oxideEndothelial NOS inhibitorDendritic cell activationNO-dependent mechanismAirway hyperresponsivenessMucus metaplasiaLymphocyte accumulationPulmonary alterationsCell hyperplasiaNOS inhibitorNormal micePhysiologic responsesCell activationInflammationENOSVEGFMiceIndependent mechanismsTissue responseLatter responseLungAngiogenesisRemodelingNull mutation
2005
ERK1/2 mitogen-activated protein kinase selectively mediates IL-13–induced lung inflammation and remodeling in vivo
Lee PJ, Zhang X, Shan P, Ma B, Lee CG, Homer RJ, Zhu Z, Rincon M, Mossman BT, Elias JA. ERK1/2 mitogen-activated protein kinase selectively mediates IL-13–induced lung inflammation and remodeling in vivo. Journal Of Clinical Investigation 2005, 116: 163-173. PMID: 16374521, PMCID: PMC1319220, DOI: 10.1172/jci25711.Peer-Reviewed Original ResearchConceptsIL-13-induced inflammationIL-13IL-13 expressionSTAT6-independent mannerIL-13 stimulationLung inflammationSpecific chemokinesTg miceEffector responsesSystemic administrationMMP-2Alveolar remodelingInflammationLungCritical rolePotent activationTissue effectsERK1/2 activationSTAT6ChemokinesInhibitor PD98059ERK1/2ERK1/2 mitogenRemodelingDiseaseRole of Cathepsin S-Dependent Epithelial Cell Apoptosis in IFN-γ-Induced Alveolar Remodeling and Pulmonary Emphysema
Zheng T, Kang MJ, Crothers K, Zhu Z, Liu W, Lee CG, Rabach LA, Chapman HA, Homer RJ, Aldous D, DeSanctis G, Underwood S, Graupe M, Flavell RA, Schmidt JA, Elias JA. Role of Cathepsin S-Dependent Epithelial Cell Apoptosis in IFN-γ-Induced Alveolar Remodeling and Pulmonary Emphysema. The Journal Of Immunology 2005, 174: 8106-8115. PMID: 15944319, DOI: 10.4049/jimmunol.174.12.8106.Peer-Reviewed Original ResearchConceptsNull mutationEpithelial cell apoptosisCell apoptosisDNA injuryTissue remodelingProtease accumulationCaspase inhibitorsMitochondrial apoptosis pathway activationDeath receptorsPropidium iodide stainingCathepsin SHuman diseasesApoptosis responseApoptosis pathway activationApoptosis inhibitionCaspase-3ApoptosisIodide stainingPathway activationCathepsin S inhibitionMutationsRemodelingCritical eventsAlveolar remodelingIFN-gamma
2000
CONSEQUENCES OF LONG-TERM INFLAMMATION Airway Remodeling
Homer R, Elias J. CONSEQUENCES OF LONG-TERM INFLAMMATION Airway Remodeling. Clinics In Chest Medicine 2000, 21: 331-343. PMID: 10907592, DOI: 10.1016/s0272-5231(05)70270-7.Peer-Reviewed Original ResearchConceptsAirway remodelingAirway chronic inflammationEffect of therapyAirway inflammationAsthmatic patientsAppropriate therapyChronic inflammationClinical manifestationsSmooth muscleCollagen depositionExperimental modelMucus glandsBiologic dataRemodelingAirwayInflammationTherapyAsthmaticsAsthmaPatientsNoncollagenous matrix