2012
Susceptibility to Progressive Cryptococcus neoformans Pulmonary Infection Is Regulated by Loci on Mouse Chromosomes 1 and 9
Carroll SF, Lafferty EI, Flaczyk A, Fujiwara TM, Homer R, Morgan K, Loredo-Osti JC, Qureshi ST. Susceptibility to Progressive Cryptococcus neoformans Pulmonary Infection Is Regulated by Loci on Mouse Chromosomes 1 and 9. Infection And Immunity 2012, 80: 4167-4176. PMID: 22988020, PMCID: PMC3497416, DOI: 10.1128/iai.00417-12.Peer-Reviewed Original ResearchConceptsC3H/HeN miceCBA/J miceHeN micePulmonary infectionJ miceFungal burdenSusceptible C3H/HeN miceInterleukin-5Cryptococcus neoformans Pulmonary InfectionIL-13 protein expressionHigher pulmonary expressionLung fungal burdenGoblet cell metaplasiaTh2 immune responsePathogenesis of pneumoniaIL-17 proteinCBA/JCryptococcal pneumoniaGreater airwayTissue neutrophiliaCryptococcal infectionCell metaplasiaIntratracheal infectionPulmonary inflammationTissue eosinophilia
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
Pulmonary 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 mediatorHypertrophy
2000
Endogenous and Exogenous IL-6 Inhibit Aeroallergen-Induced Th2 Inflammation
Wang J, Homer R, Chen Q, Elias J. Endogenous and Exogenous IL-6 Inhibit Aeroallergen-Induced Th2 Inflammation. The Journal Of Immunology 2000, 165: 4051-4061. PMID: 11034416, DOI: 10.4049/jimmunol.165.7.4051.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, IntranasalAerosolsAllergensAnimalsBronchial HyperreactivityChemokinesCytokinesGene Expression RegulationInflammationInterleukin-6LungMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred CBAMice, KnockoutMice, TransgenicOvalbuminPlethysmography, Whole BodyPulmonary EosinophiliaRNA, MessengerTh2 CellsVascular Cell Adhesion Molecule-1ConceptsIL-6Wild-type miceIL-13 proteinTh2 inflammationBronchoalveolar lavageIL-4IL-5IFN-gammaSensitized wild-type miceIL-6-deficient miceMonocyte chemoattractant protein-1Exaggerated airway responseTh2-dominated inflammationBALB/c backgroundInflammatory protein-1alphaChemoattractant protein-1IL-6 productionExogenous IL-6Endothelial VCAM-1Airway responsesAirway responsivenessAsthmatic airwaysExaggerated inflammationDeficient miceVCAM-1IL-11 Selectively Inhibits Aeroallergen-Induced Pulmonary Eosinophilia and Th2 Cytokine Production
Wang J, Homer R, Hong L, Cohn L, Lee C, Jung S, Elias J. IL-11 Selectively Inhibits Aeroallergen-Induced Pulmonary Eosinophilia and Th2 Cytokine Production. The Journal Of Immunology 2000, 165: 2222-2231. PMID: 10925310, DOI: 10.4049/jimmunol.165.4.2222.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, InhalationAerosolsAllergensAnimalsBronchoalveolar Lavage FluidCytokinesGene Expression RegulationHumansImmunizationInterleukin-11MiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred CBAMice, TransgenicMucinsMucusOvalbuminPulmonary EosinophiliaRecombinant ProteinsRespiratory MucosaSpecies SpecificityTh2 CellsTurkeysVascular Cell Adhesion Molecule-1ConceptsTh2 cell accumulationIL-11OVA challengeMucus hypersecretionIL-4IL-5VCAM-1Cell accumulationMucin 5AC (MUC5AC) gene expressionVCAM-1 gene expressionAg-specific IgEBronchoalveolar lavage (BAL) inflammationLung IL-4Th2 cytokine productionIFN-gamma productionEndothelial-cell VCAM-1IL-13 mRNAIL-13 proteinChemoattractant protein 2Chemoattractant protein-3Mucus metaplasiaTh1 inflammationPulmonary eosinophiliaTh2 inflammationAirway inflammation