2014
IL-6 Receptor α Defines Effector Memory CD8+ T Cells Producing Th2 Cytokines and Expanding in Asthma
Lee N, You S, Shin MS, Lee WW, Kang KS, Kim SH, Kim WU, Homer RJ, Kang MJ, Montgomery RR, Dela Cruz CS, Shaw AC, Lee PJ, Chupp GL, Hwang D, Kang I. IL-6 Receptor α Defines Effector Memory CD8+ T Cells Producing Th2 Cytokines and Expanding in Asthma. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 1383-1394. PMID: 25390970, PMCID: PMC4299645, DOI: 10.1164/rccm.201403-0601oc.Peer-Reviewed Original ResearchConceptsEffector memory CD8EM CD8T cellsPeripheral bloodMemory CD8IL-13IL-5IL-6RαTh2-type cytokine IL-5Different T cell subsetsLevels of GATA3Frequency of ILT cell subsetsTh2-type cytokinesHealthy control subjectsRespiratory syncytial virusT cell populationsCytokines IL-5IL-6 receptor αIL-6Rα expressionHuman peripheral bloodEffector CD8Syncytial virusTh2 cytokinesCell subsets
2012
IL-13 receptor α2-arginase 2 pathway mediates IL-13-induced pulmonary hypertension
Cho WK, Lee CM, Kang MJ, Huang Y, Giordano FJ, Lee PJ, Trow TK, Homer RJ, Sessa WC, Elias JA, Lee CG. IL-13 receptor α2-arginase 2 pathway mediates IL-13-induced pulmonary hypertension. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2012, 304: l112-l124. PMID: 23125252, PMCID: PMC3543640, DOI: 10.1152/ajplung.00101.2012.Peer-Reviewed Original ResearchConceptsPulmonary hypertensionIL-13Human pulmonary artery smooth muscle cellsDevelopment of PHPulmonary artery smooth muscle cellsRight ventricle systolic pressurePathogenesis of PHArtery smooth muscle cellsExpression of ARG2Pulmonary arterial hypertensionPulmonary vascular remodelingVentricle systolic pressurePotential therapeutic targetIL-13 treatmentSmooth muscle cellsNull mutant miceArterial hypertensionEffector cytokinesMedial thickeningSystolic pressureHemodynamic changesPulmonary arterySmall-interfering RNAVascular remodelingArginase-2
2008
IL-13 Receptor α2 Selectively Inhibits IL-13-Induced Responses in the Murine Lung
Zheng T, Liu W, Oh SY, Zhu Z, Hu B, Homer RJ, Cohn L, Grusby MJ, Elias JA. IL-13 Receptor α2 Selectively Inhibits IL-13-Induced Responses in the Murine Lung. The Journal Of Immunology 2008, 180: 522-529. PMID: 18097054, DOI: 10.4049/jimmunol.180.1.522.Peer-Reviewed Original ResearchConceptsIL-13Ralpha2Pulmonary inflammationIL-13Inflammatory responseMurine lungHigh-affinity IL-13 receptorsTransgenic IL-13IL-13 receptor α2Production of chemokinesEnhanced inflammatory responseIL-13 receptorMucus metaplasiaTh2 inflammationAirway remodelingSubepithelial fibrosisIL-4Receptor α2Critical cytokineIL-13Ralpha1IL-4RalphaDecoy receptorPhysiologic responsesInflammationTissue effectsReceptors
2007
Inhibition of NF-κB Activation Reduces the Tissue Effects of Transgenic IL-13
Chapoval SP, Al-Garawi A, Lora JM, Strickland I, Ma B, Lee PJ, Homer RJ, Ghosh S, Coyle AJ, Elias JA. Inhibition of NF-κB Activation Reduces the Tissue Effects of Transgenic IL-13. The Journal Of Immunology 2007, 179: 7030-7041. PMID: 17982094, DOI: 10.4049/jimmunol.179.10.7030.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsApoptosisCaspasesHeterocyclic Compounds, 3-RingI-kappa B KinaseInflammationInhibitor of Apoptosis ProteinsInterleukin-13MiceMice, Mutant StrainsMice, TransgenicMucusNF-kappa B p50 SubunitPeptidesPulmonary AlveoliPulmonary FibrosisPyridinesReceptors, Cell SurfaceRespiratory HypersensitivitySignal TransductionTh2 CellsConceptsTransgenic IL-13IL-13Alveolar remodelingIL-13 transgenic miceNF-kappaBMajor Th2 cytokinesExcessive mucus productionTissue effectsNF-κB activationNF-kappaB activationNF-kappaB activityNF-kappaB componentsAirway hyperresponsivenessTh2 cytokinesTissue inflammationPharmacologic approachesMucus productionIL-13Ralpha1Murine lungSmall molecule inhibitorsTissue alterationsNF-kappaB.MiceCell apoptosisDiminished levelsIncreased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice
Bhandari V, Choo-Wing R, Homer RJ, Elias JA. Increased Hyperoxia-Induced Mortality and Acute Lung Injury in IL-13 Null Mice. The Journal Of Immunology 2007, 178: 4993-5000. PMID: 17404281, DOI: 10.4049/jimmunol.178.8.4993.Peer-Reviewed Original ResearchConceptsEndogenous IL-13Acute lung injuryIL-13Lung injuryIL-13RNull miceHyperoxic acute lung injuryInhibition of injuryBronchoalveolar lavage fluidInduction of inflammationEndothelial cell growth factorVascular endothelial cell growth factorIL-13 locusCell growth factorTh2 inflammationLavage fluidIL-6Tissue inflammationVariety of diseasesIL-13Ralpha1Diseased lungsIL-4RalphaInflammationInjuryIL-11Developmental differences in the responses of IL-6 and IL-13 transgenic mice exposed to hyperoxia
Choo-Wing R, Nedrelow JH, Homer RJ, Elias JA, Bhandari V. Developmental differences in the responses of IL-6 and IL-13 transgenic mice exposed to hyperoxia. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2007, 293: l142-l150. PMID: 17400600, DOI: 10.1152/ajplung.00434.2006.Peer-Reviewed Original ResearchConceptsIL-13 transgenic miceIL-6Transgenic miceTracheal aspirate levelsWild-type littermate controlsIL-6 levelsRespiratory distress syndromeAngiogenic factor expressionLung injuryDistress syndromePremature neonatesTracheal aspiratesAdverse outcomesIL-13Human neonatesProtective effectSurvival advantageLittermate controlsAdult miceClinical relevanceTUNEL stainingCytoprotective effectsNewborn animalsMature miceFactor expression
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 pathwayRemodelingState of the Art. Mechanistic Heterogeneity in Chronic Obstructive Pulmonary Disease
Elias JA, Kang MJ, Crothers K, Homer R, Lee CG. State of the Art. Mechanistic Heterogeneity in Chronic Obstructive Pulmonary Disease. Annals Of The American Thoracic Society 2006, 3: 494-498. PMID: 16921126, DOI: 10.1513/pats.200603-068ms.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseVascular endothelial growth factorSecretory leukocyte proteinase inhibitorTh1/Tc1Obstructive pulmonary diseaseAlveolar destructionIFN-gammaMatrix metalloproteinasesMucus metaplasiaPulmonary diseaseCCR5-dependent mechanismEmphysematous alveolar destructionCigarette smoke exposureCytokine IFN-gammaIFN-gamma responsesEndothelial growth factorApoptosis-independent pathwayCCR5/Pulmonary fibrosisPulmonary responseSmoke exposureIL-13CC chemokinesFibrotic responseMurine lungTransgenic Modeling of Transforming Growth Factor-β1
Lee CG, Kang HR, Homer RJ, Chupp G, Elias JA. Transgenic Modeling of Transforming Growth Factor-β1. Annals Of The American Thoracic Society 2006, 3: 418-423. PMID: 16799085, PMCID: PMC2658706, DOI: 10.1513/pats.200602-017aw.Peer-Reviewed Original ResearchConceptsTissue fibrosisMucus metaplasiaIL-13Alveolar remodelingSpecific chemokine receptorsTransforming Growth Factor-β1Vascular endothelial growth factorGrowth factor-β1Endothelial growth factorEosinophilic inflammationTh2 responsesVascular responsesChemokine receptorsCC chemokinesPathologic fibrosisMurine lungEpithelial apoptosisFactor-β1Transgenic miceFibrosisPotent stimulatorAdenosine metabolismIL-11Transgenic modelingInflammationRole of CCR5 in the Pathogenesis of IL-13-Induced Inflammation and Remodeling
Ma B, Liu W, Homer RJ, Lee PJ, Coyle AJ, Lora JM, Lee CG, Elias JA. Role of CCR5 in the Pathogenesis of IL-13-Induced Inflammation and Remodeling. The Journal Of Immunology 2006, 176: 4968-4978. PMID: 16585593, DOI: 10.4049/jimmunol.176.8.4968.Peer-Reviewed Original ResearchConceptsIL-13-induced inflammationIL-13IL-13-induced tissue responsesMIP-1alpha/CCL3IL-13 inhibitionTransgenic IL-13Expression of CCR5Role of CCR5Tissue remodelingMatrix metalloproteinase-9MIP-1beta/CCL4CCR5 chemokine receptorInflammatory cell apoptosisIL-13 stimulationSelect chemokinesTh2 inflammationRespiratory failureCCR5 expressionChemokine receptorsMetalloproteinase-9Murine lungCCR5Alveolar remodelingCCR5 inductionInflammationRole of Early Growth Response-1 (Egr-1) in Interleukin-13-induced Inflammation and Remodeling*
Cho SJ, Kang MJ, Homer RJ, Kang HR, Zhang X, Lee PJ, Elias JA, Lee CG. Role of Early Growth Response-1 (Egr-1) in Interleukin-13-induced Inflammation and Remodeling*. Journal Of Biological Chemistry 2006, 281: 8161-8168. PMID: 16439363, DOI: 10.1074/jbc.m506770200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBronchoalveolar LavageCaspasesCell DeathCollagenDNAEarly Growth Response Protein 1Enzyme InhibitorsFibrosisFlavonoidsImmunoblottingIn Situ Nick-End LabelingInflammationInterleukin-13LungMatrix Metalloproteinase 9MiceMice, Inbred C57BLMice, TransgenicMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Models, BiologicalModels, StatisticalRNARNA, MessengerSTAT6 Transcription FactorTh2 CellsTime FactorsTransforming Growth Factor betaTransforming Growth Factor beta1TransgenesConceptsIL-13Early growth response 1IL-13-induced tissue responsesEgr-1Transgenic IL-13Matrix metalloproteinase-9Wild-type miceResponse 1Th2 inflammationCXC chemokinesMetalloproteinase-9Type miceMetalloproteinase-1Transgenic miceAlveolar remodelingTissue inhibitorInflammationPotent stimulatorImportant stimulatorMiceTissue effectsKey roleTissue responsePathogenesisApoptosis regulator
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 mitogenRemodelingDiseaseIL-11 Receptor α in the Pathogenesis of IL-13-Induced Inflammation and Remodeling
Chen Q, Rabach L, Noble P, Zheng T, Lee CG, Homer RJ, Elias JA. IL-11 Receptor α in the Pathogenesis of IL-13-Induced Inflammation and Remodeling. The Journal Of Immunology 2005, 174: 2305-2313. PMID: 15699166, DOI: 10.4049/jimmunol.174.4.2305.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChemokines, CCFibroblastsHyaluronic AcidHyperoxiaInflammationInterleukin-11Interleukin-11 Receptor alpha SubunitInterleukin-13Interleukin-13 Receptor alpha1 SubunitLungMatrix MetalloproteinasesMetaplasiaMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMucinsProtein SubunitsPulmonary AlveoliPulmonary FibrosisReceptors, InterleukinReceptors, Interleukin-11Receptors, Interleukin-13Respiratory InsufficiencySignal TransductionTransforming Growth Factor betaTransforming Growth Factor beta1ConceptsIL-13-induced inflammationIL-13IL-11IL-11RalphaIL-13-induced tissue responsesPotent stimulatorTransgenic IL-13Tissue effectsWild-type miceHyaluronic acid accumulationMucus metaplasiaTh2 inflammationRespiratory failureInflammatory disordersGob-5Major stimulatorCC chemokinesMyofibroblast accumulationInflammationTransgenic miceAlveolar remodelingReceptor αMatrix metalloproteinasesMiceDependent pathway
2004
The C10/CCL6 Chemokine and CCR1 Play Critical Roles in the Pathogenesis of IL-13-Induced Inflammation and Remodeling
Ma B, Zhu Z, Homer RJ, Gerard C, Strieter R, Elias JA. The C10/CCL6 Chemokine and CCR1 Play Critical Roles in the Pathogenesis of IL-13-Induced Inflammation and Remodeling. The Journal Of Immunology 2004, 172: 1872-1881. PMID: 14734772, DOI: 10.4049/jimmunol.172.3.1872.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCathepsinsChemokine CCL2Chemokines, CCDown-RegulationImmune SeraInflammationInterleukin-13LungLung ComplianceLung Volume MeasurementsMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMice, Inbred C57BLMice, KnockoutMice, TransgenicProtease InhibitorsPulmonary AlveoliReceptors, CCR1Receptors, ChemokineUp-RegulationConceptsIL-13-induced inflammationMatrix metalloproteinase-2IL-13Potent stimulatorMMP-9Alveolar remodelingMonocyte chemoattractant protein-1Transgenic IL-13Inflammatory protein-1alphaChemoattractant protein-1Wild-type miceIL-13 stimulationPulmonary phenotypeLevels of mRNAMetalloproteinase-4Murine lungMetalloproteinase-2Tissue inhibitorInflammationTargeted null mutationCompliance alterationsPathogenesisCCL6ChemokinesProtein 1
2003
Cytokine regulation of IL-13Rα2 and IL-13Rα1 in vivo and in vitro
Zheng T, Zhu Z, Liu W, Lee CG, Chen Q, Homer RJ, Elias JA. Cytokine regulation of IL-13Rα2 and IL-13Rα1 in vivo and in vitro. Journal Of Allergy And Clinical Immunology 2003, 111: 720-728. PMID: 12704349, DOI: 10.1067/mai.2003.1383.Peer-Reviewed Original ResearchConceptsIL-13Ralpha1 mRNAIL-13IL-13Ralpha2IL-13Ralpha1IL-4IFN-gammaRegulatory eventsTransgenic IL-13Epithelial cellsIL-13 responsesMRNA accumulationAirway epithelial cellsSites of inflammationIL-13 signalsIL-13 stimulationHigh-affinity receptorIL-10Lung fragmentsControl miceOverexpression miceIL-13Rα2Cytokine regulationIL-4RalphaIL-13Rα1Receptor subunits
2002
Interleukin-13 Mediates a Fundamental Pathway for Airway Epithelial Mucus Induced by CD4 T Cells and Interleukin-9
Whittaker L, Niu N, Temann U, Stoddard A, Flavell RA, Ray A, Homer RJ, Cohn L. Interleukin-13 Mediates a Fundamental Pathway for Airway Epithelial Mucus Induced by CD4 T Cells and Interleukin-9. American Journal Of Respiratory Cell And Molecular Biology 2002, 27: 593-602. PMID: 12397019, DOI: 10.1165/rcmb.4838.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCells, CulturedGene Expression RegulationInterferon-gammaInterleukin-13Interleukin-9LungMiceMice, Inbred BALB CMice, Mutant StrainsMice, TransgenicMucin 5ACMucinsNF-kappa BReceptors, InterferonReceptors, Interleukin-4Recombinant ProteinsRespiratory MucosaSignal TransductionTh2 CellsConceptsIL-13Th2 cellsTh2-induced airway inflammationEpithelial mucusCD4 Th cellsCD4 T cellsAbsence of interleukinIL-13 actsNuclear factor-kappaBAsthma resultsTh2 effectsAirway inflammationMucus hyperproductionNegative infectionsTh cytokinesInflammatory cellsRecipient miceTh cellsIL-4IL-5Respiratory tractAirway epitheliumIL-9T cellsComplete blockadeOverlapping and enzyme-specific contributions of matrix metalloproteinases-9 and -12 in IL-13–induced inflammation and remodeling
Lanone S, Zheng T, Zhu Z, Liu W, Lee CG, Ma B, Chen Q, Homer RJ, Wang J, Rabach LA, Rabach ME, Shipley JM, Shapiro SD, Senior RM, Elias JA. Overlapping and enzyme-specific contributions of matrix metalloproteinases-9 and -12 in IL-13–induced inflammation and remodeling. Journal Of Clinical Investigation 2002, 110: 463-474. PMID: 12189240, PMCID: PMC150413, DOI: 10.1172/jci14136.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell MovementChemotaxis, LeukocyteCytokinesEndopeptidasesFibrosisInflammationInterleukin-13LungLung ComplianceLung DiseasesMatrix Metalloproteinase 12Matrix Metalloproteinase 9MetalloendopeptidasesMiceMice, KnockoutMice, TransgenicPulmonary AlveoliRespiratory InsufficiencyRespiratory MucosaConceptsIL-13-induced inflammationMMP-9IL-13MMP-12MMP-2Respiratory failureAlveolar remodelingMatrix metalloproteinasesIL-13 transgenic miceMMP-12-deficient miceAccumulation of eosinophilsBronchoalveolar lavage fluidIL-13 actsIL-13 inductionMatrix metalloproteinases-9Recovery of leukocytesLung enlargementLymphocytic inflammationNeutrophil accumulationLymphocyte recoveryLavage fluidTotal leukocytesInflammatory effectsAlveolar enlargementMetalloproteinases-9Transgenic Overexpression of Interleukin (IL)-10 in the Lung Causes Mucus Metaplasia, Tissue Inflammation, and Airway Remodeling via IL-13-dependent and -independent Pathways*
Lee CG, Homer RJ, Cohn L, Link H, Jung S, Craft JE, Graham BS, Johnson TR, Elias JA. Transgenic Overexpression of Interleukin (IL)-10 in the Lung Causes Mucus Metaplasia, Tissue Inflammation, and Airway Remodeling via IL-13-dependent and -independent Pathways*. Journal Of Biological Chemistry 2002, 277: 35466-35474. PMID: 12107190, DOI: 10.1074/jbc.m206395200.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceChloride ChannelsCloning, MolecularDNA PrimersFluorescent Antibody TechniqueGene Expression RegulationIn Situ HybridizationInflammationInterleukin-10Interleukin-13LungMiceMice, TransgenicMolecular Sequence DataMucoproteinsMucous MembranePhenotypePolymerase Chain ReactionReceptors, Interleukin-4STAT6 Transcription FactorTrans-ActivatorsConceptsMucus metaplasiaIL-10Tissue inflammationIL-13Tumor necrosis factor productionIL-13/ILLipopolysaccharide-induced inflammationNecrosis factor productionAirway fibrosisNeutrophil accumulationAirway remodelingSubepithelial fibrosisGob-5Levels of mRNAMetaplasiaInflammationTransgenic miceFibrosisSTAT-6Effector propertiesTransgenic overexpressionFactor productionMiceInterleukinMultiple mechanismsPulmonary type II cell hypertrophy and pulmonary lipoproteinosis are features of chronic IL-13 exposure
Homer RJ, Zheng T, Chupp G, He S, Zhu Z, Chen Q, Ma B, Hite RD, Gobran LI, Rooney SA, Elias JA. Pulmonary type II cell hypertrophy and pulmonary lipoproteinosis are features of chronic IL-13 exposure. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2002, 283: l52-l59. PMID: 12060560, DOI: 10.1152/ajplung.00438.2001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAsthmaBronchoalveolar Lavage FluidGene ExpressionHypertrophyImmunohistochemistryInterleukin-13MiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicProteolipidsPulmonary AlveoliPulmonary FibrosisPulmonary Surfactant-Associated Protein APulmonary Surfactant-Associated ProteinsPulmonary SurfactantsRNA, MessengerConceptsType II cell hypertrophyIL-13Cell hypertrophyChronic pulmonary conditionsPathogenesis of asthmaBronchoalveolar lavage fluidTh2-mediated immunityIL-13 exposureProminent interstitial fibrosisWild-type miceAirway hyperresponsivenessMucus metaplasiaEosinophilic inflammationPulmonary diseaseInterstitial fibrosisLavage fluidPulmonary conditionsTwo- to threefold increaseSurfactant accumulationLittermate controlsPotent stimulatorSurfactant phospholipidsFibrosisKey mediatorHypertrophyIL-13-Induced Chemokine Responses in the Lung: Role of CCR2 in the Pathogenesis of IL-13-Induced Inflammation and Remodeling
Zhu Z, Ma B, Zheng T, Homer RJ, Lee CG, Charo IF, Noble P, Elias JA. IL-13-Induced Chemokine Responses in the Lung: Role of CCR2 in the Pathogenesis of IL-13-Induced Inflammation and Remodeling. The Journal Of Immunology 2002, 168: 2953-2962. PMID: 11884467, DOI: 10.4049/jimmunol.168.6.2953.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBronchoalveolar Lavage FluidCells, CulturedChemokine CCL2Chemokines, CCEndopeptidasesHyaluronic AcidInflammationInterleukin-13LungLung ComplianceMetaplasiaMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMinkMucusPhenotypeProtease InhibitorsPulmonary AlveoliPulmonary FibrosisReceptors, CCR2Receptors, ChemokineRespiratory InsufficiencyRespiratory MucosaRNA, MessengerTotal Lung CapacityTransforming Growth Factor betaTransforming Growth Factor beta1ConceptsMonocyte chemotactic proteinTransgenic IL-13IL-13Potent stimulatorIL-13 transgenic miceIL-13-induced inflammationSecretory leukocyte proteinase inhibitorRole of CCR2Macrophage-derived chemokineActivation-regulated chemokineMacrophage inflammatory proteinHyaluronic acid accumulationPathogenesis of humanMucus metaplasiaCCR2 deficiencyRespiratory failureChemokine responsesPulmonary inflammationLung complianceMIP-2Lavage fluidMIP-1betaEotaxin-2MCP-1MIP-3alpha