2014
Pulmonary Fibrosis
Murray L, Homer R, Gulati M, Herzog E. Pulmonary Fibrosis. 2014, 2636-2653. DOI: 10.1016/b978-0-12-386456-7.05307-7.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsInterstitial lung diseasePulmonary fibrosisLung fibrosisConnective tissue disease-related interstitial lung diseaseIdiopathic pulmonary fibrosisSalient clinical featuresDistinctive pathological featuresWound healing responseClinical featuresChronic injuryLung diseasePathological featuresCirculating BiomarkersInflammatory responseLung parenchymaCertain therapiesPathogenic mechanismsScar tissueClinical monitoringFibrosisHealing responseFatal natureGenetic formsDiseasePotential role
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
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
Idiopathic pulmonary fibrosis: new insights into pathogenesis
Noble PW, Homer RJ. Idiopathic pulmonary fibrosis: new insights into pathogenesis. Clinics In Chest Medicine 2004, 25: 749-758. PMID: 15564020, DOI: 10.1016/j.ccm.2004.04.003.Peer-Reviewed Original ResearchConceptsUsual interstitial pneumoniaInterstitial pneumoniaUncontrolled lung inflammationUnique pathologic featuresProgressive clinical courseAnti-inflammatory therapyIdiopathic pulmonary fibrosisLung inflammationClinical coursePathologic featuresPulmonary fibrosisCardinal manifestationsInflammatory responseNew therapiesFibroblast functionPneumoniaPathogenesisTherapyCurrent thoughtsRecent reviewBiopsyInflammationFibrosisIPFActivation of the STAT pathway in acute lung injury
Severgnini M, Takahashi S, Rozo LM, Homer RJ, Kuhn C, Jhung JW, Perides G, Steer M, Hassoun PM, Fanburg BL, Cochran BH, Simon AR. Activation of the STAT pathway in acute lung injury. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2004, 286: l1282-l1292. PMID: 14729509, DOI: 10.1152/ajplung.00349.2003.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsCells, CulturedDisease Models, AnimalDNA-Binding ProteinsHydrochloric AcidInterleukin-6Janus Kinase 2KineticsLipopolysaccharidesLiverLungMaleMiceMice, Inbred BALB CMice, Inbred C57BLMitogen-Activated Protein KinasesOxidation-ReductionPancreatitisProtein-Tyrosine KinasesProto-Oncogene ProteinsRespiratory Distress SyndromeRespiratory MucosaSrc-Family KinasesSTAT3 Transcription FactorTrans-ActivatorsTumor Necrosis Factor-alphaConceptsAcute lung injuryIL-6Lung injuryLPS treatmentDevastating clinical problemGastric acid aspirationIntranasal LPS administrationResident lung cellsSTAT3 activationAcute pancreatitis modelSTAT activationAcid aspirationLPS administrationCytokine responsesInflammatory cellsInflammatory responsePancreatitis modelClinical problemMultiple organsLungLung cellsLPSEndothelial cellsTranscription factorsCritical mediator
2000
Interferon γ Induction of Pulmonary Emphysema in the Adult Murine Lung
Wang Z, Zheng T, Zhu Z, Homer R, Riese R, Chapman H, Shapiro S, Elias J. Interferon γ Induction of Pulmonary Emphysema in the Adult Murine Lung. Journal Of Experimental Medicine 2000, 192: 1587-1600. PMID: 11104801, PMCID: PMC2193095, DOI: 10.1084/jem.192.11.1587.Peer-Reviewed Original ResearchConceptsAdult murine lungMurine lungProtease/antiprotease balanceChronic obstructive pulmonary diseaseSecretory leukocyte proteinase inhibitorNeutrophil-rich inflammationObstructive pulmonary diseaseInterferon γ inductionPulmonary diseasePulmonary complianceChronic inflammationInflammatory responseLung volumePulmonary emphysemaPulmonary tissueΓ inductionAlveolar enlargementMMP-9Matrix metalloproteinaseEmphysemaLungInflammationSelective inhibitionProminent proteaseMacrophages
1999
T Helper 1 Cells and Interferon γ Regulate Allergic Airway Inflammation and Mucus Production
Cohn L, Homer R, Niu N, Bottomly K. T Helper 1 Cells and Interferon γ Regulate Allergic Airway Inflammation and Mucus Production. Journal Of Experimental Medicine 1999, 190: 1309-1318. PMID: 10544202, PMCID: PMC2195688, DOI: 10.1084/jem.190.9.1309.Peer-Reviewed Original ResearchConceptsTh1 cellsTh2 cellsMucus productionAirway eosinophiliaIFN-gammaRecipient miceAirway inflammationIFN-gamma receptor signalingT helper type 1T helper 1 cellsAllergic airway inflammationTh2 cytokine secretionHelper type 1Different inhibitory pathwaysAsthmatic patientsPathologic featuresCytokine secretionInflammatory responseRespiratory tractEosinophiliaInhibitory pathwaysMouse modelInflammationType 1Marked reductionPulmonary 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
1996
Targeted expression of IL-11 in the murine airway causes lymphocytic inflammation, bronchial remodeling, and airways obstruction.
Tang W, Geba GP, Zheng T, Ray P, Homer RJ, Kuhn C, Flavell RA, Elias JA. Targeted expression of IL-11 in the murine airway causes lymphocytic inflammation, bronchial remodeling, and airways obstruction. Journal Of Clinical Investigation 1996, 98: 2845-2853. PMID: 8981933, PMCID: PMC507752, DOI: 10.1172/jci119113.Peer-Reviewed Original ResearchMeSH KeywordsAirway ObstructionAirway ResistanceAnimalsBlotting, NorthernBlotting, SouthernCloning, MolecularDisease Models, AnimalGene Expression RegulationHistocytochemistryImmunohistochemistryInterleukin-11LungMethacholine ChlorideMiceMice, TransgenicMicroscopy, ElectronPromoter Regions, GeneticProteinsPulmonary FibrosisUteroglobinConceptsIL-11Fibrotic responseTransgene miceAlpha-smooth muscle actinMononuclear cell infiltratePotential effector functionsSmooth muscle actinTargeted expressionSmooth muscle cellsHuman airway disordersType IIILung stromal cellsAirway disordersLymphocytic inflammationCell infiltrateSubepithelial fibrosisAirway resistanceRespiratory virusesMouse airwaysMurine airwaysInflammatory fociPhysiologic evaluationInflammatory responseBronchial remodelingMHC class