2008
Enhanced Innate Immune Responsiveness to Pulmonary Cryptococcus neoformans Infection Is Associated with Resistance to Progressive Infection
Guillot L, Carroll SF, Homer R, Qureshi ST. Enhanced Innate Immune Responsiveness to Pulmonary Cryptococcus neoformans Infection Is Associated with Resistance to Progressive Infection. Infection And Immunity 2008, 76: 4745-4756. PMID: 18678664, PMCID: PMC2546841, DOI: 10.1128/iai.00341-08.Peer-Reviewed Original ResearchConceptsSJL/J miceKC/CXCL1Cryptococcus neoformans infectionC. neoformans infectionKeratinocyte-derived chemokineNeoformans infectionJ miceInnate immune responseTNF-alphaProgressive infectionImmune responseResistant SJL/J miceMIP-2/CXCL2Pulmonary C. neoformans infectionPulmonary Cryptococcus neoformans infectionPulmonary innate immune responseSJL/J macrophagesC. neoformansInflammatory cytokine tumor necrosis factor alphaEnhanced innate immune responseMIP-1alpha/CCL3IL-12/ILMCP-1/CCL2Cytokine tumor necrosis factor alphaTumor necrosis factor alpha
2007
A Novel Pathway That Regulates Inflammatory Disease in the Respiratory Tract
Niu N, Le Goff MK, Li F, Rahman M, Homer RJ, Cohn L. A Novel Pathway That Regulates Inflammatory Disease in the Respiratory Tract. The Journal Of Immunology 2007, 178: 3846-3855. PMID: 17339484, DOI: 10.4049/jimmunol.178.6.3846.Peer-Reviewed Original ResearchConceptsAirway inflammationInflammatory diseasesRespiratory tractTh2-induced airway inflammationChronic airway inflammatory diseaseLymphocyte-deficient miceState of immunosuppressionAcute airway inflammationAirway inflammatory diseasesEffector Th cellsTh2 cells resultsAirway hyperresponsivenessInflammation wanesTh2 modelEffector Th1Respiratory illnessTh cellsInhalational exposureInflammationInhibitory effectSuch diseasesDiseaseStriking inhibitionTh1Localized treatment
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 reductionInhibition 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 mutantTh2-induced airway mucus production is dependent on IL-4Ralpha, but not on eosinophils.
Cohn L, Homer RJ, MacLeod H, Mohrs M, Brombacher F, Bottomly K. Th2-induced airway mucus production is dependent on IL-4Ralpha, but not on eosinophils. The Journal Of Immunology 1999, 162: 6178-83. PMID: 10229862, DOI: 10.4049/jimmunol.162.10.6178.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, InhalationAnimalsAsthmaBronchiEosinophiliaEosinophilsInterleukin-13 Receptor alpha1 SubunitInterleukin-4Interleukin-5Mast CellsMiceMice, Inbred BALB CMice, Inbred C57BLMice, Mutant StrainsMice, TransgenicMucusOvalbuminReceptors, InterleukinReceptors, Interleukin-13Receptors, Interleukin-4Th2 CellsConceptsMucus productionTh2 cellsAirway eosinophiliaAirway inflammationIL-4RalphaAirway mucus productionCD4 Th2 cellsAirway obstructionBAL eosinophiliaHuman asthmaticsMucus hyperproductionClinical symptomsIL-13Recipient miceTh1 cellsIL-4IL-5Respiratory tractEosinophiliaMast cellsAnimal modelsEosinophilsMarked increaseCell stimulationMucus
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