2020
The Pulmonary Metatranscriptome Prior to Pediatric Hematopoietic Cell Transplantation Identifies Post-HCT Lung Injury
Zinter MS, Lindemans C, Versluys B, Mayday MY, Sunshine S, Reyes G, Sirota M, Sapru A, Matthay MA, Kharbanda S, Dvorak CC, Boelens J, DeRisi JL. The Pulmonary Metatranscriptome Prior to Pediatric Hematopoietic Cell Transplantation Identifies Post-HCT Lung Injury. Blood 2020, 137: 1679-1689. PMID: 33512420, PMCID: PMC7995292, DOI: 10.1182/blood.2020009246.Peer-Reviewed Original ResearchConceptsHematopoietic cell transplantationLung injuryHCT candidatesBronchoalveolar lavagePediatric allogeneic hematopoietic cell transplantationAllogeneic hematopoietic cell transplantationRespiratory viral loadUniversity Medical Center UtrechtInnate immune activationPulmonary gene expressionLong-term survivalSeparate validation cohortT cell activationCumulative incidenceBAL fluidViral loadDisastrous complicationImmune activationValidation cohortCell transplantationLung healthMucus productionHigh incidenceIndependent cohortInjuryMechanisms of Epithelial Immunity Evasion by Respiratory Bacterial Pathogens
Sharma L, Feng J, Britto CJ, Dela Cruz CS. Mechanisms of Epithelial Immunity Evasion by Respiratory Bacterial Pathogens. Frontiers In Immunology 2020, 11: 91. PMID: 32117248, PMCID: PMC7027138, DOI: 10.3389/fimmu.2020.00091.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsBacterial lung infectionsImmune cellsBacterial clearanceRespiratory bacterial pathogensEpithelial cellsLung infectionSecretion of cytokinesEpithelial host defenseMuco-ciliary clearanceHuge economic burdenRespiratory epithelial cellsLung epithelial surfaceMajor healthcare challengeEpithelial immune mechanismsBacterial pathogensAntimicrobial peptide productionImmune mechanismsImmune protectionMucus productionEconomic burdenPathogen clearanceEpithelial immunityHost defenseClinical researchEpithelial resistance
2015
Glutathione Reaction Products with a Chemical Allergen, Methylene-diphenyl Diisocyanate, Stimulate Alternative Macrophage Activation and Eosinophilic Airway Inflammation
Wisnewski AV, Liu J, Colangelo CM. Glutathione Reaction Products with a Chemical Allergen, Methylene-diphenyl Diisocyanate, Stimulate Alternative Macrophage Activation and Eosinophilic Airway Inflammation. Chemical Research In Toxicology 2015, 28: 729-737. PMID: 25635619, PMCID: PMC4667722, DOI: 10.1021/tx5005002.Peer-Reviewed Original ResearchConceptsEosinophilic inflammatory responseAlternative macrophage activationInflammatory responseChemical allergensMacrophage activationAirway eosinophil numbersEosinophilic airway inflammationInnate immune responseGreater inflammatory responseAirway levelsMDI conjugationAirway inflammationOccupational asthmaIL-12MDI exposureAsthma pathogenesisEosinophil numbersNaïve miceAirway fluidRespiratory tractImmune responseMucus productionSkin exposureMDI conjugatesVivo evidence
2014
NLRP6 Inflammasome Orchestrates the Colonic Host-Microbial Interface by Regulating Goblet Cell Mucus Secretion
Wlodarska M, Thaiss CA, Nowarski R, Henao-Mejia J, Zhang JP, Brown EM, Frankel G, Levy M, Katz MN, Philbrick WM, Elinav E, Finlay BB, Flavell RA. NLRP6 Inflammasome Orchestrates the Colonic Host-Microbial Interface by Regulating Goblet Cell Mucus Secretion. Cell 2014, 156: 1045-1059. PMID: 24581500, PMCID: PMC4017640, DOI: 10.1016/j.cell.2014.01.026.Peer-Reviewed Original ResearchConceptsRegulatory pathwaysGoblet cell mucus secretionHost-microbial mutualismHost-microbial interfaceNLRP6 inflammasomeMucus secretionGoblet cellsBiogeographical distributionProkaryotic cellsInnate immune playersNLRP6 deficiencyGranule exocytosisImmune regulatory pathwaysInflammasome-deficient miceColonic microbiota compositionLarge intestinal lumenCritical orchestratorsImmune playersPersistent infectionMucus productionCellsIntestinal lumenPathwayMucosal surfacesMicrobiota composition
2010
Th2 LCR is essential for regulation of Th2 cytokine genes and for pathogenesis of allergic asthma
Koh BH, Hwang SS, Kim JY, Lee W, Kang MJ, Lee CG, Park JW, Flavell RA, Lee GR. Th2 LCR is essential for regulation of Th2 cytokine genes and for pathogenesis of allergic asthma. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 10614-10619. PMID: 20483988, PMCID: PMC2890814, DOI: 10.1073/pnas.1005383107.Peer-Reviewed Original ResearchConceptsCD4 T cellsAllergic asthmaTh2 cytokine genesCytokine genesKO miceT cellsNaïve CD4 T cellsLung airway inflammationSerum IgE levelsBronchoalveolar lavage fluidRecruitment of eosinophilsWild-type miceAirway hyperresponsivenessOvalbumin challengeAirway inflammationIgE levelsLavage fluidTh2 cytokinesAirway wallMucus productionMouse modelAsthmaMarked reductionCre-loxP recombinationMiceAirway 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
Advances in Mucous Cell Metaplasia
Curran DR, Cohn L. Advances in Mucous Cell Metaplasia. American Journal Of Respiratory Cell And Molecular Biology 2009, 42: 268-275. PMID: 19520914, PMCID: PMC2830403, DOI: 10.1165/rcmb.2009-0151tr.BooksConceptsMucous cell metaplasiaCell metaplasiaMucous metaplasiaChronic obstructive pulmonary diseaseChronic airway diseasesObstructive pulmonary diseaseExacerbation of asthmaChronic airwayAirway obstructionAirway diseaseMucus hypersecretionPulmonary diseaseMolecular mechanismsHarmful insultsIL-13MUC5AC expressionEpidermal growth factor receptor (EGFR) activationGoblet cell granulesGrowth factor receptor activationMucin productionMucus productionNew therapiesGoblet cellsFront-line protectionMetaplasia
2008
Endogenous IL-11 Signaling Is Essential in Th2- and IL-13–Induced Inflammation and Mucus Production
Lee CG, Hartl D, Matsuura H, Dunlop FM, Scotney PD, Fabri LJ, Nash AD, Chen NY, Tang CY, Chen Q, Homer RJ, Baca M, Elias JA. Endogenous IL-11 Signaling Is Essential in Th2- and IL-13–Induced Inflammation and Mucus Production. American Journal Of Respiratory Cell And Molecular Biology 2008, 39: 739-746. PMID: 18617680, PMCID: PMC2586049, DOI: 10.1165/rcmb.2008-0053oc.Peer-Reviewed Original ResearchConceptsIL-13 productionMucus productionIL-11Th2 inflammationIL-11RalphaAerosol antigen challengeAirway mucus productionBronchoalveolar lavage (BAL) inflammationPulmonary Th2 responsesLevels of IgEIL-13 responsesEndogenous IL-11Null mutant miceBAL inflammationMucus metaplasiaEosinophilic inflammationTh2 responsesAntigen challengeIL-11 receptorWT miceTh2 cytokinesIntraperitoneal administrationInflammationMucus responseMurine lung
2007
Inhibition of NF-κB Activation Reduces the Tissue Effects of Transgenic IL-13
Chapoval SP, Al-Garawi A, Lora JM, Strickland I, Ma B, Lee PJ, Homer RJ, Ghosh S, Coyle AJ, Elias JA. Inhibition of NF-κB Activation Reduces the Tissue Effects of Transgenic IL-13. The Journal Of Immunology 2007, 179: 7030-7041. PMID: 17982094, DOI: 10.4049/jimmunol.179.10.7030.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsApoptosisCaspasesHeterocyclic Compounds, 3-RingI-kappa B KinaseInflammationInhibitor of Apoptosis ProteinsInterleukin-13MiceMice, Mutant StrainsMice, TransgenicMucusNF-kappa B p50 SubunitPeptidesPulmonary AlveoliPulmonary FibrosisPyridinesReceptors, Cell SurfaceRespiratory HypersensitivitySignal TransductionTh2 CellsConceptsTransgenic IL-13IL-13Alveolar remodelingIL-13 transgenic miceNF-kappaBMajor Th2 cytokinesExcessive mucus productionTissue effectsNF-κB activationNF-kappaB activationNF-kappaB activityNF-kappaB componentsAirway hyperresponsivenessTh2 cytokinesTissue inflammationPharmacologic approachesMucus productionIL-13Ralpha1Murine lungSmall molecule inhibitorsTissue alterationsNF-kappaB.MiceCell apoptosisDiminished levelsRecombinant basic fibroblast growth factor inhibits the airway hyperresponsiveness, mucus production, and lung inflammation induced by an allergen challenge
Jeon SG, Lee CG, Oh MH, Chun EY, Gho YS, Cho SH, Kim JH, Min KU, Kim YY, Kim YK, Elias JA. Recombinant basic fibroblast growth factor inhibits the airway hyperresponsiveness, mucus production, and lung inflammation induced by an allergen challenge. Journal Of Allergy And Clinical Immunology 2007, 119: 831-837. PMID: 17289133, DOI: 10.1016/j.jaci.2006.12.653.Peer-Reviewed Original ResearchConceptsAsthma mouse modelLung inflammationBasic fibroblast growth factorAsthma phenotypesMucus productionFibroblast growth factorAllergen challengeTg miceRecombinant FGF2Therapeutic effectMouse modelWild-type control miceGrowth factorDevelopment of AHRTGF-beta1 miceRegional lymph nodesWhole-body plethysmographyDevelopment of asthmaBronchoalveolar lavage cellularityRecombinant basic fibroblast growth factorFGF2-deficient micePeriodic acid-Schiff stainingFGF2 mRNA expressionRole of FGF2Acid-Schiff staining
2006
IL9 leads to airway inflammation by inducing IL13 expression in airway epithelial cells
Temann UA, Laouar Y, Eynon EE, Homer R, Flavell RA. IL9 leads to airway inflammation by inducing IL13 expression in airway epithelial cells. International Immunology 2006, 19: 1-10. PMID: 17101709, DOI: 10.1093/intimm/dxl117.Peer-Reviewed Original ResearchConceptsAirway epithelial cellsLung inflammationTg miceEnhanced lung inflammationEosinophilic lung inflammationEpithelial cellsMast cell hyperplasiaAsthma-like phenotypeRecombinase-activating genes 1IL13 levelsMucus hypersecretionCell hyperplasiaInflammatory cytokinesLung pathologyLung sectionsT cellsMast cellsMucus productionIL13 expressionB cellsLung epitheliumTransgenic miceInflammationIL13Lung
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
Cytokine Regulation of Mucus Production in a Model of Allergic Asthma
Cohn L, Whittaker L, Niu N, Homer RJ. Cytokine Regulation of Mucus Production in a Model of Allergic Asthma. Novartis Foundation Symposia 2002, 248: 201-220. PMID: 12568496, DOI: 10.1002/0470860790.ch13.BooksMeSH KeywordsAdministration, InhalationAnimalsAsthmaBronchoalveolar Lavage FluidCells, CulturedExocytosisGene Expression RegulationImmunizationInterferon-gammaInterferonsInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-4Interleukin-5Interleukin-9Mast CellsMiceMice, TransgenicModels, AnimalMucinsMucusOvalbuminPeptide FragmentsPulmonary EosinophiliaRadiation ChimeraReceptors, Antigen, T-Cell, alpha-betaReceptors, InterleukinReceptors, Interleukin-13Receptors, Interleukin-4Respiratory SystemSignal TransductionTh1 CellsTh2 CellsConceptsAirway inflammationTh2 cellsMucus productionTh1 cellsT cell receptor transgenic CD4Airway inflammatory infiltrateDifferent lymphocyte subsetsBone marrow chimerasAbsence of interleukinAirway obstructionAllergic asthmaLymphocyte subsetsEosinophilic inflammationMucus hyperproductionInflammatory infiltrateClinical symptomsInflammatory cellsTh2 lymphocytesRecipient miceTh cellsTransgenic CD4Respiratory tractMast cellsCytokine regulationInflammation
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
1997
Induction of Airway Mucus Production By T Helper 2 (Th2) Cells: A Critical Role For Interleukin 4 In Cell Recruitment But Not Mucus Production
Cohn L, Homer R, Marinov A, Rankin J, Bottomly K. Induction of Airway Mucus Production By T Helper 2 (Th2) Cells: A Critical Role For Interleukin 4 In Cell Recruitment But Not Mucus Production. Journal Of Experimental Medicine 1997, 186: 1737-1747. PMID: 9362533, PMCID: PMC2199146, DOI: 10.1084/jem.186.10.1737.Peer-Reviewed Original ResearchConceptsTh2 cellsMucus productionAirway inflammationIL-4Asthmatic patientsCell recruitmentOVA-specific Th2 cellsT helper 2 cellsIL-4-deficient miceAirway mucus productionOVA-specific TCRRole of Th1CD4 T cellsImportant clinical symptomInduction of inflammationTh2 cell recruitmentCD4 Th1Airway biopsiesClinical symptomsTh1 cellsTNF-alphaT cellsInterleukin-4Effector functionsMucus secretion
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