2009
Cutting Edge: Limiting MHC Class II Expression to Dendritic Cells Alters the Ability to Develop Th2- Dependent Allergic Airway Inflammation
Niu N, Laufer T, Homer RJ, Cohn L. Cutting Edge: Limiting MHC Class II Expression to Dendritic Cells Alters the Ability to Develop Th2- Dependent Allergic Airway Inflammation. The Journal Of Immunology 2009, 183: 1523-1527. PMID: 19596982, DOI: 10.4049/jimmunol.0901349.Peer-Reviewed Original ResearchConceptsAllergic airway inflammationMHC class II expressionAirway inflammationDendritic cellsClass II expressionTh2 generationTh2 immunityTh2-dependent allergic airway inflammationTh1 immune responseIFN-gamma productionAirway neutrophiliaTh2 primingRespiratory tractTh2 cellsImmune responseClass II signalsInflammationTh2 recruitmentMice resultsMiceCells altersImmunityActivationCellsNeutrophilia
2004
Airway hyper‐reactivity mediated by B‐1 cell immunoglobulin M antibody generating complement C5a at 1 day post‐immunization in a murine hapten model of non‐atopic asthma
Kawikova I, Paliwal V, Szczepanik M, Itakura A, Fukui M, Campos RA, Geba GP, Homer RJ, Iliopoulou BP, Pober JS, Tsuji RF, Askenase PW. Airway hyper‐reactivity mediated by B‐1 cell immunoglobulin M antibody generating complement C5a at 1 day post‐immunization in a murine hapten model of non‐atopic asthma. Immunology 2004, 113: 234-245. PMID: 15379984, PMCID: PMC1782564, DOI: 10.1111/j.1365-2567.2004.01936.x.Peer-Reviewed Original ResearchConceptsAirflow obstructionImmune cellsC5a receptor-deficient miceSubsequent airway challengeNon-atopic asthmaReceptor-deficient miceImmunoglobulin M antibodiesIgM-producing cellsWild-type miceIgM monoclonal antibodyAirway reactivityHapten challengeHapten modelAirway challengeMethacholine challengeAsthma modelSkin immunizationLymph nodesNaive miceNaïve recipientsM antibodiesDays postimmunizationSubsequent airwayMale miceComplement C5a
2002
Cytokine Regulation of Mucus Production in a Model of Allergic Asthma
Cohn L, Whittaker L, Niu N, Homer RJ. Cytokine Regulation of Mucus Production in a Model of Allergic Asthma. Novartis Foundation Symposia 2002, 248: 201-220. PMID: 12568496, DOI: 10.1002/0470860790.ch13.BooksMeSH KeywordsAdministration, InhalationAnimalsAsthmaBronchoalveolar Lavage FluidCells, CulturedExocytosisGene Expression RegulationImmunizationInterferon-gammaInterferonsInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-4Interleukin-5Interleukin-9Mast CellsMiceMice, TransgenicModels, AnimalMucinsMucusOvalbuminPeptide FragmentsPulmonary EosinophiliaRadiation ChimeraReceptors, Antigen, T-Cell, alpha-betaReceptors, InterleukinReceptors, Interleukin-13Receptors, Interleukin-4Respiratory SystemSignal TransductionTh1 CellsTh2 CellsConceptsAirway inflammationTh2 cellsMucus productionTh1 cellsT cell receptor transgenic CD4Airway inflammatory infiltrateDifferent lymphocyte subsetsBone marrow chimerasAbsence of interleukinAirway obstructionAllergic asthmaLymphocyte subsetsEosinophilic inflammationMucus hyperproductionInflammatory infiltrateClinical symptomsInflammatory cellsTh2 lymphocytesRecipient miceTh cellsTransgenic CD4Respiratory tractMast cellsCytokine regulationInflammation
2001
IL-11: Insights in asthma from overexpression transgenic modeling
Zheng T, Zhu Z, Wang J, Homer R, Elias J. IL-11: Insights in asthma from overexpression transgenic modeling. Journal Of Allergy And Clinical Immunology 2001, 108: 489-496. PMID: 11590369, DOI: 10.1067/mai.2001.118510.Peer-Reviewed Original ResearchConceptsIL-11Potential effector functionsMajor basic proteinMurine findingsAirway obstructionSevere asthmaAsthmatic airwaysSubepithelial fibrosisMononuclear infiltrateTissue inflammationFibroblast supernatantsAlveolar developmentVirus infectionPlatelet reconstitutionEffector functionsNonrespiratory tissuesExaggerated quantitiesTransgenic miceDisease severityVariety of stimuliStructural cellsImportant stimulatorSoluble factorsTransgenic modelingEpithelial cells
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 ResearchMeSH KeywordsAnimalsAsthmaBronchiCytokinesHumansInflammationMuscle, SmoothRegional Blood FlowRespiratory SystemTime FactorsConceptsAirway remodelingAirway chronic inflammationEffect of therapyAirway inflammationAsthmatic patientsAppropriate therapyChronic inflammationClinical manifestationsSmooth muscleCollagen depositionExperimental modelMucus glandsBiologic dataRemodelingAirwayInflammationTherapyAsthmaticsAsthmaPatientsNoncollagenous matrix
1999
Airway remodeling in asthma
Elias J, Zhu Z, Chupp G, Homer R. Airway remodeling in asthma. Journal Of Clinical Investigation 1999, 104: 1001-1006. PMID: 10525034, PMCID: PMC408860, DOI: 10.1172/jci8124.Peer-Reviewed Original ResearchPulmonary 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