2011
RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism
Ma B, Dela Cruz CS, Hartl D, Kang MJ, Takyar S, Homer RJ, Lee CG, Elias JA. RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism. American Journal Of Respiratory And Critical Care Medicine 2011, 183: 1322-1335. PMID: 21278304, PMCID: PMC3114061, DOI: 10.1164/rccm.201008-1276oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDEAD Box Protein 58DEAD-box RNA HelicasesDisease Models, AnimalEdemaFocal Adhesion Protein-Tyrosine KinasesImmunity, InnateInflammationInterferon Type IMiceMice, TransgenicMitogen-Activated Protein KinasesNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasePoly I-CPulmonary Disease, Chronic ObstructiveToll-Like Receptor 3Vascular Endothelial Growth Factor AConceptsVascular endothelial growth factorType 2 inflammationChronic obstructive pulmonary disease exacerbationsObstructive pulmonary disease exacerbationsChronic obstructive pulmonary diseaseViral pathogen-associated molecular patternsEndothelial nitric oxide synthaseRIG-like helicasePulmonary disease exacerbationsObstructive pulmonary diseasePathogenesis of asthmaRespiratory syncytial virusNormal pulmonary physiologyNitric oxide synthaseAntiviral innate immunityPathogen-associated molecular patternsReceptor-dependent pathwayTissue responseEndothelial growth factorVEGF receptor 1Ability of VEGFDisease exacerbationPulmonary diseaseRespiratory virusesControl mice
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
1999
Inhibition of Allergic Inflammation in a Murine Model of Asthma by Expression of a Dominant-Negative Mutant of GATA-3
Zhang D, Yang L, Cohn L, Parkyn L, Homer R, Ray P, Ray A. Inhibition of Allergic Inflammation in a Murine Model of Asthma by Expression of a Dominant-Negative Mutant of GATA-3. Immunity 1999, 11: 473-482. PMID: 10549629, DOI: 10.1016/s1074-7613(00)80122-3.Peer-Reviewed Original ResearchMeSH KeywordsAerosolsAmino Acid SubstitutionAnimalsAsthmaBronchoalveolar Lavage FluidDNA-Binding ProteinsDrug HypersensitivityEosinophiliaGATA3 Transcription FactorGene Expression RegulationGenes, DominantImmunizationImmunoglobulin EInflammationInterleukin-13Interleukin-4Interleukin-5LungMiceMice, Inbred C57BLMice, TransgenicMucusMutagenesis, Site-DirectedOvalbuminTh2 CellsTrans-ActivatorsConceptsCytokines IL-4GATA-3IL-13IL-4IL-5Th2 cytokines IL-4Pathogenesis of asthmaTreatment of asthmaTranscription factor GATA-3Potential therapeutic targetAirway eosinophiliaTh2 responsesAllergic inflammationAllergic diseasesTh2 cytokinesT-cell-specific fashionTh1 cellsIgE synthesisTh2 cellsMucus productionMurine modelTherapeutic targetTransgenic miceAsthmaDominant negative mutant
1998
Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation
Yang L, Cohn L, Zhang D, Homer R, Ray A, Ray P. Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation. Journal Of Experimental Medicine 1998, 188: 1739-1750. PMID: 9802985, PMCID: PMC2212522, DOI: 10.1084/jem.188.9.1739.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigensAsthmaBase SequenceChemokine CCL11Chemokines, CCCytokinesDNA PrimersEosinophiliaGene ExpressionInflammationIntercellular Adhesion Molecule-1Interleukin-4Interleukin-5LungMiceMice, Inbred C57BLMice, KnockoutNF-kappa BNF-kappa B p50 SubunitOvalbuminReverse Transcriptase Polymerase Chain ReactionTh2 CellsVascular Cell Adhesion Molecule-1ConceptsAirway inflammationEosinophil-rich airway inflammationTh2 cytokine interleukin-5Adhesion molecules VCAM-1Chemokine macrophage inflammatory proteinCell adhesion molecule VCAM-1Allergic airway inflammationEosinophilic airway inflammationT cell primingPathogenesis of asthmaT helper 2T cell recruitmentInduction of eosinophiliaMacrophage inflammatory proteinCytokines interleukin-5Wild-type miceSites of inflammationNuclear factor κBAllergic asthmaAsthmatic airwaysHelper 2Cell primingInflammatory proteinMIP-1betaExtravasation of eosinophils