2008
Acidic Mammalian Chitinase Is Secreted via an ADAM17/Epidermal Growth Factor Receptor-dependent Pathway and Stimulates Chemokine Production by Pulmonary Epithelial Cells*
Hartl D, He CH, Koller B, Da Silva CA, Homer R, Lee CG, Elias JA. Acidic Mammalian Chitinase Is Secreted via an ADAM17/Epidermal Growth Factor Receptor-dependent Pathway and Stimulates Chemokine Production by Pulmonary Epithelial Cells*. Journal Of Biological Chemistry 2008, 283: 33472-33482. PMID: 18824549, PMCID: PMC2586247, DOI: 10.1074/jbc.m805574200.Peer-Reviewed Original ResearchConceptsEpidermal growth factor receptorLung epithelial cellsAcidic mammalian chitinaseChemokine productionEpithelial cellsT helper cell type 2 inflammationEpidermal growth factor receptor-dependent pathwayAsthma-like responsesType 2 inflammationMammalian chitinaseEpithelial cell productionReceptor-dependent pathwayPulmonary epithelial cellsEGFR-dependent pathwayGrowth factor receptorCotransfection experimentsEffector responsesParacrine fashionEGFR inhibitionSecretionFactor receptorA549 cellsAMCaseRecombinant AMCaseRegulatory effects
2007
IL-18 Is Induced and IL-18 Receptor α Plays a Critical Role in the Pathogenesis of Cigarette Smoke-Induced Pulmonary Emphysema and Inflammation
Kang MJ, Homer RJ, Gallo A, Lee CG, Crothers KA, Cho SJ, Rochester C, Cain H, Chupp G, Yoon HJ, Elias JA. IL-18 Is Induced and IL-18 Receptor α Plays a Critical Role in the Pathogenesis of Cigarette Smoke-Induced Pulmonary Emphysema and Inflammation. The Journal Of Immunology 2007, 178: 1948-1959. PMID: 17237446, DOI: 10.4049/jimmunol.178.3.1948.Peer-Reviewed Original ResearchConceptsChronic obstructive lung diseaseObstructive lung diseaseIL-18Wild-type miceCigarette smokeLung diseasePulmonary emphysemaIL-18RalphaPathogenesis of CSEffects of CSAir-exposed miceIL-18 pathwayIL-18 receptor αIL-18R signalingTh1 inflammationPulmonary macrophagesEpithelial apoptosisReceptor αInflammationPotent stimulatorEmphysemaCaspase-1MiceCritical roleElevated levels
2006
IL9 leads to airway inflammation by inducing IL13 expression in airway epithelial cells
Temann UA, Laouar Y, Eynon EE, Homer R, Flavell RA. IL9 leads to airway inflammation by inducing IL13 expression in airway epithelial cells. International Immunology 2006, 19: 1-10. PMID: 17101709, DOI: 10.1093/intimm/dxl117.Peer-Reviewed Original ResearchConceptsAirway epithelial cellsLung inflammationTg miceEnhanced lung inflammationEosinophilic lung inflammationEpithelial cellsMast cell hyperplasiaAsthma-like phenotypeRecombinase-activating genes 1IL13 levelsMucus hypersecretionCell hyperplasiaInflammatory cytokinesLung pathologyLung sectionsT cellsMast cellsMucus productionIL13 expressionB cellsLung epitheliumTransgenic miceInflammationIL13Lung
2005
Regulation of lung injury and repair by Toll-like receptors and hyaluronan
Jiang D, Liang J, Fan J, Yu S, Chen S, Luo Y, Prestwich GD, Mascarenhas MM, Garg HG, Quinn DA, Homer RJ, Goldstein DR, Bucala R, Lee PJ, Medzhitov R, Noble PW. Regulation of lung injury and repair by Toll-like receptors and hyaluronan. Nature Medicine 2005, 11: 1173-1179. PMID: 16244651, DOI: 10.1038/nm1315.Peer-Reviewed Original ResearchConceptsAcute lung injuryLung injuryToll-like receptorsInflammatory responseTLR2-dependent mannerSera of individualsCell-specific overexpressionEpithelial cell apoptosisEpithelial cell integrityHyaluronan degradation productsChemokine productionInflammatory cellsTissue injuryExtracellular matrix glycosaminoglycan hyaluronanTransepithelial migrationInjuryCell surface hyaluronanHyaluronan fragmentsCell apoptosisBasal activationClearance resultsInflammationGlycosaminoglycan hyaluronanReceptorsHyaluronan
2004
Acidic Mammalian Chitinase in Asthmatic Th2 Inflammation and IL-13 Pathway Activation
Zhu Z, Zheng T, Homer RJ, Kim YK, Chen NY, Cohn L, Hamid Q, Elias JA. Acidic Mammalian Chitinase in Asthmatic Th2 Inflammation and IL-13 Pathway Activation. Science 2004, 304: 1678-1682. PMID: 15192232, DOI: 10.1126/science.1095336.Peer-Reviewed Original ResearchConceptsTh2 inflammationAcidic mammalian chitinaseIL-13-induced responsesPathway activationTh2-dominated disordersMammalian chitinaseAirway hyperresponsivenessAsthma modelT helperHuman asthmaChemokine inductionInterleukin-13Exaggerated quantitiesImportant mediatorEpithelial cellsAsthmaInflammationActivationHyperresponsivenessInfection
2000
IL-13 stimulates vascular endothelial cell growth factor and protects against hyperoxic acute lung injury
Corne J, Chupp G, Lee C, Homer R, Zhu Z, Chen Q, Ma B, Du Y, Roux F, McArdle J, Waxman A, Elias J. IL-13 stimulates vascular endothelial cell growth factor and protects against hyperoxic acute lung injury. Journal Of Clinical Investigation 2000, 106: 783-791. PMID: 10995789, PMCID: PMC381393, DOI: 10.1172/jci9674.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodiesBlotting, WesternBronchoalveolar Lavage FluidEndothelial Growth FactorsEpithelial CellsFibroblast Growth Factor 10Fibroblast Growth Factor 7Fibroblast Growth FactorsGene Expression RegulationGrowth SubstancesHyperoxiaImmunohistochemistryInterleukin-13LungLymphokinesMacrophagesMiceMice, TransgenicMuscle, SmoothOxygenProtein IsoformsSurvival RateVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsAcute lung injuryHyperoxic acute lung injuryIL-13Lung injuryVEGF accumulationProtective effectTransgenic miceRoom airNontransgenic littermate controlsBreathing room airAcid isoformEndothelial cell growth factorVascular endothelial cell growth factorMice breathing room airCell growth factorBronchoalveolar lavageNontransgenic miceLittermate controlsImportant causeAntibody neutralizationMiceGrowth factorInjuryHyperoxiaSurvival
1999
Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production
Zhu Z, Homer R, Wang Z, Chen Q, Geba G, Wang J, Zhang Y, Elias J. Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production. Journal Of Clinical Investigation 1999, 103: 779-788. PMID: 10079098, PMCID: PMC408149, DOI: 10.1172/jci5909.Peer-Reviewed Original ResearchConceptsMucus cell metaplasiaAirway hyperresponsivenessIL-13Airway fibrosisCell metaplasiaPulmonary expressionCharcot-LeydenInflammatory responseBaseline airway resistanceSubepithelial airway fibrosisTransgene-negative littermatesVivo effector functionNonspecific airway hyperresponsivenessTransgene-positive miceEosinophilic inflammatory responseEpithelial cell hypertrophyGranulocyte-macrophage colony-stimulating factorTransgene-positive animalsColony-stimulating factorClara cell 10Cause inflammationMucus hypersecretionSubepithelial fibrosisAirway resistanceEotaxin production