2011
The Role of TSLP in IL-13-Induced Atopic March
Zhu Z, Oh MH, Yu J, Liu YJ, Zheng T. The Role of TSLP in IL-13-Induced Atopic March. Scientific Reports 2011, 1: 23. PMID: 22355542, PMCID: PMC3251897, DOI: 10.1038/srep00023.Peer-Reviewed Original ResearchConceptsThymic stromal lymphopoietinAtopic dermatitisAtopic marchAirway hyperresponsivenessLevels of TSLPRole of TSLPIL-13 transgenic miceAcute atopic dermatitisAllergic asthma responsesChronic atopic dermatitisHuman atopic dermatitisImmune cell productionSkin of miceSystemic Th2 immunityAD skinAsthma responseLung inflammationMucus hypersecretionTh2 immunitySerum IgE.Th2 cytokinesIL-13AD phenotypeTransgenic miceDependent mechanism
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
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 miceInflammationIL13LungCysteinyl Leukotrienes Regulate Th2 Cell-Dependent Pulmonary Inflammation
Kim DC, Hsu FI, Barrett NA, Friend DS, Grenningloh R, Ho IC, Al-Garawi A, Lora JM, Lam BK, Austen KF, Kanaoka Y. Cysteinyl Leukotrienes Regulate Th2 Cell-Dependent Pulmonary Inflammation. The Journal Of Immunology 2006, 176: 4440-4448. PMID: 16547282, DOI: 10.4049/jimmunol.176.7.4440.Peer-Reviewed Original ResearchConceptsPulmonary inflammationDelayed-type cutaneous hypersensitivityAg-specific IgECys-LT generationSmooth muscle constrictorTh2 cell cytokinesGoblet cell hyperplasiaIntraepithelial mast cellsCytokine mRNA expressionCell-dependent responsesAirway hyperresponsivenessOVA sensitizationWild-type controlsCutaneous hypersensitivityCys-LTsMucus hypersecretionEosinophil infiltrationCell hyperplasiaCysteinyl leukotrienesCell cytokinesInflammatory responseMast cellsInflammationChallenge protocolMRNA expression
2003
Differential roles for CD4 and CD8 T cells after diisocyanate sensitization: Genetic control of TH2-induced lung inflammation
Herrick CA, Das J, Xu L, Wisnewski AV, Redlich CA, Bottomly K. Differential roles for CD4 and CD8 T cells after diisocyanate sensitization: Genetic control of TH2-induced lung inflammation. Journal Of Allergy And Clinical Immunology 2003, 111: 1087-1094. PMID: 12743574, DOI: 10.1067/mai.2003.1413.Peer-Reviewed Original ResearchConceptsContact hypersensitivityT cellsAirway eosinophiliaAirway inflammationBALB/c miceDiisocyanate-induced asthmaCD8 T cellsLung inflammatory responseMajor effector cellsIL-13 productionMeans of inhalationNovel mouse modelEpicutaneous exposureAtopic asthmaLung inflammationMucus hypersecretionOccupational asthmaEpicutaneous sensitizationEffector cellsCytokine productionC miceIL-5Serum antibodiesInflammatory responseC57BL/10 mice
2002
A novel mouse model of diisocyanate-induced asthma showing allergic-type inflammation in the lung after inhaled antigen challenge
Herrick CA, Xu L, Wisnewski AV, Das J, Redlich CA, Bottomly K. A novel mouse model of diisocyanate-induced asthma showing allergic-type inflammation in the lung after inhaled antigen challenge. Journal Of Allergy And Clinical Immunology 2002, 109: 873-878. PMID: 11994714, DOI: 10.1067/mai.2002.123533.Peer-Reviewed Original ResearchConceptsDiisocyanate-induced asthmaNovel mouse modelLung inflammationMouse modelAirway eosinophiliaAntigen challengeHuman asthmaAntigen-induced lung inflammationBALB/c miceAllergic-type inflammationLung inflammatory cellsCytokine-deficient miceVigorous inflammatory responsePrevious mouse modelsAtopic asthmaMucus hypersecretionOccupational asthmaContact hypersensitivityInflammatory cellsC miceInflammatory responseType cytokinesIFN-gammaAsthmaHuman diseasesRecent 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
2000
IL-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
1999
Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production
Zhu Z, Homer R, Wang Z, Chen Q, Geba G, Wang J, Zhang Y, Elias J. Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production. Journal Of Clinical Investigation 1999, 103: 779-788. PMID: 10079098, PMCID: PMC408149, DOI: 10.1172/jci5909.Peer-Reviewed Original ResearchConceptsMucus cell metaplasiaAirway hyperresponsivenessIL-13Airway fibrosisCell metaplasiaPulmonary expressionCharcot-LeydenInflammatory responseBaseline airway resistanceSubepithelial airway fibrosisTransgene-negative littermatesVivo effector functionNonspecific airway hyperresponsivenessTransgene-positive miceEosinophilic inflammatory responseEpithelial cell hypertrophyGranulocyte-macrophage colony-stimulating factorTransgene-positive animalsColony-stimulating factorClara cell 10Cause inflammationMucus hypersecretionSubepithelial fibrosisAirway resistanceEotaxin production
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