2017
Bile acids initiate cholestatic liver injury by triggering a hepatocyte-specific inflammatory response
Cai SY, Ouyang X, Chen Y, Soroka CJ, Wang J, Mennone A, Wang Y, Mehal WZ, Jain D, Boyer JL. Bile acids initiate cholestatic liver injury by triggering a hepatocyte-specific inflammatory response. JCI Insight 2017, 2: e90780. PMID: 28289714, PMCID: PMC5333973, DOI: 10.1172/jci.insight.90780.Peer-Reviewed Original ResearchConceptsLiver injuryInflammatory responseBile acid-induced liver injuryCholestatic liver injuryInflammatory liver injuryProinflammatory cytokine expressionCholestatic liver diseaseBile duct ligationVivo mouse modelHepatic infiltrationInflammatory injurySerum aminotransferasesLiver diseaseCholestatic patientsCytokine expressionChemokine inductionPathophysiologic concentrationsNeutrophil chemotaxisDuct ligationPathophysiologic levelsMouse modelNew therapiesInnate immunityInjuryPeriportal areas
2014
Immune Chaperone gp96 Drives the Contributions of Macrophages to Inflammatory Colon Tumorigenesis
Morales C, Rachidi S, Hong F, Sun S, Ouyang X, Wallace C, Zhang Y, Garret-Mayer E, Wu J, Liu B, Li Z. Immune Chaperone gp96 Drives the Contributions of Macrophages to Inflammatory Colon Tumorigenesis. Cancer Research 2014, 74: 446-459. PMID: 24322981, PMCID: PMC4002507, DOI: 10.1158/0008-5472.can-13-1677.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow CellsCell Transformation, NeoplasticColitisColonColonic NeoplasmsCrosses, GeneticCytokinesDisease ProgressionDNA RepairGene DeletionGene Expression Regulation, NeoplasticInflammationInterleukin-17Interleukin-23MacrophagesMaleMembrane GlycoproteinsMiceMice, KnockoutMucous MembraneConceptsDNA repair machineryDNA repair pathwaysColon tumorigenesisTumor-associated macrophagesRepair machineryRepair pathwaysOncogenic programEndoplasmic reticulumMutation rateChaperone gp96Β-cateninColon cancerMechanistic underpinningsCellular sitesTumorigenesisReduced expressionEpithelial cellsGenotoxic natureToll-like receptorsInflammation-associated colon cancerImportant driverGp96Inflammation-associated colon tumorigenesisCritical inflammatory cytokinesExpression
2013
Inflammasome biology in fibrogenesis
Ouyang X, Ghani A, Mehal WZ. Inflammasome biology in fibrogenesis. Biochimica Et Biophysica Acta 2013, 1832: 979-988. PMID: 23562491, DOI: 10.1016/j.bbadis.2013.03.020.Peer-Reviewed Original ResearchMeSH KeywordsCytokinesHumansInflammasomesInterleukin-1betaToll-Like ReceptorsTumor Necrosis Factor-alphaConceptsInflammatory pathwaysInflammatory responseTissue injuryToll-like receptor agonistsAssociation of TGFPro-fibrotic pathwaysDownstream inflammatory cytokinesCytokines interleukin-1βAcute inflammatory responseTumor necrosis factorLiver stellate cellsNew therapeutic targetsNumber of organsTissue macrophage populationsIL-18Inflammatory cytokinesInterleukin-1βReceptor agonistFibrogenic responseImmune cellsNecrosis factorSterile insultsStellate cellsTherapeutic targetMacrophage populations
2010
Potentiation of Th17 cytokines in aging process contributes to the development of colitis
Ouyang X, Yang Z, Zhang R, Arnaboldi P, Lu G, Li Q, Wang W, Zhang B, Cui M, Zhang H, Liang-Chen J, Qin L, Zheng F, Huang B, Xiong H. Potentiation of Th17 cytokines in aging process contributes to the development of colitis. Cellular Immunology 2010, 266: 208-217. PMID: 21074754, PMCID: PMC3006034, DOI: 10.1016/j.cellimm.2010.10.007.Peer-Reviewed Original ResearchConceptsT cellsIL-17IL-22Aged miceTh17 cytokinesDendritic cellsYoung miceImmune responseAutoimmune/inflammatory diseasesDevelopment of colitisIL-17 productionMemory T cellsNaïve T cellsSevere colitisIL-17FInflammatory disordersInflammatory diseasesAged individualsMRNA expressionMiceColitisAged peopleSignificant differencesCytokinesHealthy ones