2014
Regulation of Nasal Airway Homeostasis and Inflammation in Mice by SHP-1 and Th2/Th1 Signaling Pathways
Cho SH, Oh SY, Lane AP, Lee J, Oh MH, Lee S, Zheng T, Zhu Z. Regulation of Nasal Airway Homeostasis and Inflammation in Mice by SHP-1 and Th2/Th1 Signaling Pathways. PLOS ONE 2014, 9: e103685. PMID: 25090641, PMCID: PMC4121172, DOI: 10.1371/journal.pone.0103685.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChemokinesEosinophiliaGelatinHomeostasisInflammationInterferon-gammaMatrix Metalloproteinase 2Matrix Metalloproteinase 9MetaplasiaMice, Inbred C57BLMice, Mutant StrainsMucusNasal Lavage FluidNasal MucosaProtein Tyrosine Phosphatase, Non-Receptor Type 6RhinitisSignal TransductionTh1 CellsTh2 CellsConceptsMatrix metalloproteinasesNasal inflammationAllergic rhinitisTh1 cytokinesInflammatory cellsTh2 cytokinesNasal airwayChronic inflammatory diseaseExpression of cytokinesTh2-skewed inflammationIFN-γ geneMucus metaplasiaTh1 paradigmAirway homeostasisInflammatory mediatorsTh2 lymphocytesImmune homeostasisInflammatory diseasesViable motheaten miceInflammationTransepithelial migrationCytokinesMev miceClearance mechanismsTh2The AGC kinase SGK1 regulates TH1 and TH2 differentiation downstream of the mTORC2 complex
Heikamp E, Patel C, Collins S, Waickman A, Oh M, Sun I, Illei P, Sharma A, Naray-Fejes-Toth A, Fejes-Toth G, Misra-Sen J, Horton M, Powell J. The AGC kinase SGK1 regulates TH1 and TH2 differentiation downstream of the mTORC2 complex. Nature Immunology 2014, 15: 457-464. PMID: 24705297, PMCID: PMC4267697, DOI: 10.1038/ni.2867.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAnimalsAsthmaCell DifferentiationCells, CulturedEndosomal Sorting Complexes Required for TransportGene Expression RegulationHepatocyte Nuclear Factor 1-alphaImmediate-Early ProteinsInterferon-gammaMechanistic Target of Rapamycin Complex 2Melanoma, ExperimentalMiceMice, Inbred C57BLMice, KnockoutMultiprotein ComplexesNedd4 Ubiquitin Protein LigasesPoxviridae InfectionsProtein Serine-Threonine KinasesT Cell Transcription Factor 1Th1 CellsTh2 CellsTOR Serine-Threonine KinasesTranscription FactorsTumor BurdenUbiquitin-Protein LigasesVaccinia virus
2013
SHP-1 Regulation of Mast Cell Function in Allergic Inflammation and Anaphylaxis
Zhou L, Oh SY, Zhou Y, Yuan B, Wu F, Oh MH, Wang Y, Takemoto C, Van Rooijen N, Zheng T, Zhu Z. SHP-1 Regulation of Mast Cell Function in Allergic Inflammation and Anaphylaxis. PLOS ONE 2013, 8: e55763. PMID: 23390550, PMCID: PMC3563592, DOI: 10.1371/journal.pone.0055763.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAllergensAnaphylaxisAnimalsBasophilsCell DifferentiationCells, CulturedCytokinesGene ExpressionInflammationInjections, IntravenousLipopolysaccharidesLungMast CellsMiceMice, KnockoutOvalbuminProtein Tyrosine Phosphatase, Non-Receptor Type 6Respiratory HypersensitivitySignal TransductionTh2 CellsConceptsTh2 immune responseAllergic inflammationAirway inflammationMast cell functionImmune responseMast cellsDeficient bone marrow cellsMast cell-deficient miceCell-deficient miceCell functionSevere allergic reactionsWild-type miceSHP-1Bone marrow cellsAirway stimulationAdoptive transferSystemic anaphylaxisAnaphylactic responseClinical symptomsImmunological homeostasisDeficient miceAllergic reactionsType miceAnaphylaxisInflammation
2012
Epicutaneous Exposure to Staphylococcal Superantigen Enterotoxin B Enhances Allergic Lung Inflammation via an IL-17A Dependent Mechanism
Yu J, Oh MH, Park JU, Myers AC, Dong C, Zhu Z, Zheng T. Epicutaneous Exposure to Staphylococcal Superantigen Enterotoxin B Enhances Allergic Lung Inflammation via an IL-17A Dependent Mechanism. PLOS ONE 2012, 7: e39032. PMID: 22848348, PMCID: PMC3407176, DOI: 10.1371/journal.pone.0039032.Peer-Reviewed Original ResearchConceptsIL-17A-dependent mechanismsAtopic dermatitisAirway hyperresponsivenessAtopic marchLung inflammationDependent mechanismDevelopment of ADSeverity of ADEnterotoxin BSystemic Th2 responseAllergic lung inflammationTh17/ILSkin barrier abnormalitiesIL-6 productionSkin of patientsEpicutaneous exposureAllergic rhinitisIL-17ATh2 responsesEpicutaneous sensitizationLymph nodesImmune environmentLesional skinAllergen ovalbuminStimulating lymphocytes
2009
SHP-1 Deficient Mast Cells Are Hyperresponsive to Stimulation and Critical in Initiating Allergic Inflammation in the Lung
Zhang L, Oh SY, Wu X, Oh MH, Wu F, Schroeder JT, Takemoto CM, Zheng T, Zhu Z. SHP-1 Deficient Mast Cells Are Hyperresponsive to Stimulation and Critical in Initiating Allergic Inflammation in the Lung. The Journal Of Immunology 2009, 184: 1180-1190. PMID: 20042576, PMCID: PMC4755278, DOI: 10.4049/jimmunol.0901972.Peer-Reviewed Original ResearchConceptsBone marrow-derived mast cellsAllergic asthma phenotypeMarrow-derived mast cellsMast cellsTh2 cytokinesMev miceAsthma phenotypesTh2 cytokines IL-4Allergic inflammatory responseTh2 cytokine productionRelease of mediatorsCytokines IL-4Mast cell productionT cells 2SHP-1 deficiencySrc homology region 2 domain-containing phosphatase-1Amount of mediatorMast cell developmentPulmonary inflammationAllergic inflammationCytokine productionTh2 phenotypeIL-13IL-4Deficient mast cells
2007
TH2 and TH1 lung inflammation induced by airway allergen sensitization with low and high doses of double-stranded RNA
Jeon SG, Oh SY, Park HK, Kim YS, Shim EJ, Lee HS, Oh MH, Bang B, Chun EY, Kim SH, Gho YS, Zhu Z, Kim YY, Kim YK. TH2 and TH1 lung inflammation induced by airway allergen sensitization with low and high doses of double-stranded RNA. Journal Of Allergy And Clinical Immunology 2007, 120: 803-812. PMID: 17610940, DOI: 10.1016/j.jaci.2007.05.030.Peer-Reviewed Original ResearchConceptsRespiratory viral infectionsAllergen sensitizationLung inflammationViral infectionAirway sensitizationIL-4Immune responseMouse modelHigh dosesIL-13-deficient miceIFN-gamma-deficient miceT-bet-deficient miceToll-like receptor 3Airway allergen exposureAllergic lung inflammationAdaptive immune responsesToll-like receptorsIL-4 expressionSTAT6-deficient miceNovel mouse modelIFN-gamma expressionAllergen exposurePathophysiologic mechanismsIL-13Deficient miceAirway Exposure Levels of Lipopolysaccharide Determine Type 1 versus Type 2 Experimental Asthma
Kim YK, Oh SY, Jeon SG, Park HW, Lee SY, Chun EY, Bang B, Lee HS, Oh MH, Kim YS, Kim JH, Gho YS, Cho SH, Min KU, Kim YY, Zhu Z. Airway Exposure Levels of Lipopolysaccharide Determine Type 1 versus Type 2 Experimental Asthma. The Journal Of Immunology 2007, 178: 5375-5382. PMID: 17404323, DOI: 10.4049/jimmunol.178.8.5375.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAnimalsAsthmaBronchial HyperreactivityFemaleHumansInterferon-gammaInterleukin-12LipopolysaccharidesMaleMiceMice, Inbred BALB CMice, Inbred C57BLMiddle AgedOvalbuminReceptors, Tumor Necrosis FactorRNA, MessengerSignal TransductionSTAT4 Transcription FactorTh1 CellsTh2 CellsTransforming Growth Factor beta1Tumor Necrosis Factor-alphaConceptsHigh-dose LPSLow-dose LPSAsthma phenotypesAdaptive immune responsesImmune responseAirway hyperresponsivenessAllergen sensitizationTNF-alpha receptor-deficient miceType 1IFN-gamma-deficient miceSevere asthma patientsReceptor-deficient miceAllergen-specific IgEExposure levelsIL-12 expressionTNF-alpha expressionIFN-gamma expressionLow LPS levelsNoneosinophilic inflammationAirway inflammationAllergic asthmaNeutrophilic inflammationSevere asthmaAirway exposureAsthma patients