2018
BPI Fold-Containing Family A Member 1 (BPIFA1) regulates lung neutrophil recruitment and interferon signaling during acute inflammation
Khanal S, Niu N, Huleihel L, Herazo-Maya J, Kaminski N, Cohn L, Britto C. BPI Fold-Containing Family A Member 1 (BPIFA1) regulates lung neutrophil recruitment and interferon signaling during acute inflammation. 2018, pa4254. DOI: 10.1183/13993003.congress-2018.pa4254.Peer-Reviewed Original Research
2010
Epithelial reticulon 4B (Nogo-B) is an endogenous regulator of Th2-driven lung inflammation
Wright PL, Yu J, Di YP, Homer RJ, Chupp G, Elias JA, Cohn L, Sessa WC. Epithelial reticulon 4B (Nogo-B) is an endogenous regulator of Th2-driven lung inflammation. Journal Of Experimental Medicine 2010, 207: 2595-2607. PMID: 20975041, PMCID: PMC2989775, DOI: 10.1084/jem.20100786.Peer-Reviewed Original ResearchConceptsLung inflammationTh2-mediated lung inflammationSevere human asthmaAsthma-like phenotypeNonallergic miceHuman asthmaInflammation resultsKO miceLung tissueNogo expressionAirway epitheliumSmooth muscleReticulon 4BTransgenic miceLung epitheliumEpithelial reconstitutionMiceMarked reductionProtective genesEndogenous regulatorNogoInflammationLungPLUNCTransgenic expressionMicrobial And Inflammatory Signals Promote Airway Inflammation By Inhibiting The Epithelial Protein PLUNC
Britto C, Curran D, Liu Q, Cohn L. Microbial And Inflammatory Signals Promote Airway Inflammation By Inhibiting The Epithelial Protein PLUNC. 2010, a1389-a1389. DOI: 10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1389.Peer-Reviewed Original ResearchAirway epithelium response to IFN-γ regulates allergic airway inflammation (91.7)
Mitchell C, Provost K, Niu N, Homer R, Cohn L. Airway epithelium response to IFN-γ regulates allergic airway inflammation (91.7). The Journal Of Immunology 2010, 184: 91.7-91.7. DOI: 10.4049/jimmunol.184.supp.91.7.Peer-Reviewed Original ResearchAirway epithelial cellsAllergic airway inflammationAllergic airway diseaseAirway eosinophiliaAirway inflammationAirway diseaseNon-hematopoietic cellsEpithelial cellsIFN-γRIFN-γ receptor-deficient miceIFN-γR expressionReceptor-deficient miceBone marrow chimerasOVA-specific Th1Th1 cellsDeficient miceMucus productionBone marrowEpithelium responseIFNMaximal inhibitionEosinophiliaInflammationMiceInhibitory effect
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 altersImmunityActivationCellsNeutrophiliaDecreased Ovalbumin-Induced Airway Inflammation in Mice Deficient in the Sensory Neuronal Ion Channel TRPA1.
Caceres A, Brackmann M, Bessac B, Sui A, Cohn L, Jordt. Decreased Ovalbumin-Induced Airway Inflammation in Mice Deficient in the Sensory Neuronal Ion Channel TRPA1. 2009, a6324. DOI: 10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6324.Peer-Reviewed Original Research
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
2004
Asthma: Mechanisms of Disease Persistence and Progression
Cohn L, Elias JA, Chupp GL. Asthma: Mechanisms of Disease Persistence and Progression. Annual Review Of Immunology 2004, 22: 789-815. PMID: 15032597, DOI: 10.1146/annurev.immunol.22.012703.104716.BooksConceptsIL-13Key effector cytokineAnti-inflammatory therapyIL-13 productionProduction of chemokinesProgression of diseaseAirway fibrosisAllergic asthmaAirway remodelingEffector cytokinesEosinophilic inflammationPersistent diseaseTh2 cytokinesEpithelial damageDisease progressionInflammatory responseTh2 cellsMucus productionSmooth muscleBronchial airwaysMatrix metalloproteinasesAnimal dataAsthmaDisease persistenceInflammation
2002
Recent Concepts in the Pathogenesis and Treatment of Asthma
Whittaker L, Cohn L. Recent Concepts in the Pathogenesis and Treatment of Asthma. Clinical Pulmonary Medicine 2002, 9: 135-144. DOI: 10.1097/00045413-200205000-00001.Peer-Reviewed Original ResearchTreatment of asthmaLow-dose antigen exposureCD4 lymphocyte subsetsSpecific proinflammatory mediatorsMainstay of therapyAirways of asthmaticsPathogenesis of asthmaAirway hyperresponsivenessAirflow obstructionLymphocyte subsetsMucus hypersecretionAntigen exposureProinflammatory mediatorsInflammatory cytokinesTh2 lymphocytesTh1 cellsCellular inflammationCommon syndromeNovel therapiesAsthmaDisease processInflammationPathogenesisΒ-agonistsContinued investigation
2001
IL-4 Promotes Airway Eosinophilia by Suppressing IFN-γ Production: Defining a Novel Role for IFN-γ in the Regulation of Allergic Airway Inflammation
Cohn L, Herrick C, Niu N, Homer R, Bottomly K. IL-4 Promotes Airway Eosinophilia by Suppressing IFN-γ Production: Defining a Novel Role for IFN-γ in the Regulation of Allergic Airway Inflammation. The Journal Of Immunology 2001, 166: 2760-2767. PMID: 11160342, DOI: 10.4049/jimmunol.166.4.2760.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, CutaneousAdministration, IntranasalAdoptive TransferAnimalsBone Marrow CellsBone Marrow TransplantationBronchiCell MovementDown-RegulationEosinophilsFemaleHematopoietic Stem CellsInflammationInterferon-gammaInterleukin-13Interleukin-4Interleukin-5MaleMiceMice, Inbred BALB CMice, KnockoutMice, TransgenicOvalbuminPulmonary EosinophiliaReceptors, InterferonRespiratory HypersensitivityTh2 CellsUp-RegulationConceptsAirway eosinophiliaIL-4IFN-gammaTh2 cellsAirway eosinophilsIL-5Allergic airway inflammationIFN-γ productionTh2 cell generationAirway inflammationEosinophilic inflammationLung eosinophiliaLung parenchymalTh2 cytokinesIntranasal administrationRespiratory tractLung tissueCounterregulatory effectsEosinophiliaCell transferEosinophilsHemopoietic cellsInflammationAirwayIFN
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 reduction