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
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
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