2021
Apobec1 complementation factor overexpression promotes hepatic steatosis, fibrosis and hepatocellular cancer
Blanc V, Riordan JD, Soleymanjahi S, Nadeau J, Nalbantoglu I, Xie Y, Molitor EA, Madison BB, Brunt EM, Mills JC, Rubin DC, Ng I, Ha Y, Roberts LR, Davidson NO. Apobec1 complementation factor overexpression promotes hepatic steatosis, fibrosis and hepatocellular cancer. Journal Of Clinical Investigation 2021, 131 PMID: 33445170, PMCID: PMC7773377, DOI: 10.1172/jci138699.Peer-Reviewed Original ResearchConceptsHuman hepatocellular cancerHigh-fructose dietHepatocellular cancerNonalcoholic fatty liver diseaseFatty liver diseaseExpression of mRNALipogenic gene expressionSpontaneous fibrosisAdvanced fibrosisLiver diseaseLiver functionHepatic steatosisInflammatory pathwaysInflammatory responseFed chowLong-term effectsTissue microarrayHepatic proliferationMRNA expressionFactor overexpressionReduced survivalFibrosisOxidative stressExtracellular matrix organizationSteatosis
2018
The impact of diet‐induced hepatic steatosis in a murine model of hepatic ischemia/reperfusion injury
Liss KHH, McCommis KS, Chambers KT, Pietka TA, Schweitzer GG, Park SL, Nalbantoglu I, Weinheimer CJ, Hall AM, Finck BN. The impact of diet‐induced hepatic steatosis in a murine model of hepatic ischemia/reperfusion injury. Liver Transplantation 2018, 24: 908-921. PMID: 29729104, PMCID: PMC6097916, DOI: 10.1002/lt.25189.Peer-Reviewed Original ResearchConceptsDiet-induced hepatic steatosisSteatotic liversHepatic steatosisReperfusion injuryLiver diseaseMicrovesicular steatosisMurine modelObesity-associated nonalcoholic fatty liver diseaseHepatic ischemia/reperfusion injuryEnd-stage liver diseaseIschemia/reperfusion injuryNonalcoholic fatty liver diseasePlasma alanine aminotransferase levelsAlanine aminotransferase levelsFatty liver diseaseCriteria donor organsInflammatory cytokine concentrationsPotential therapeutic approachHepatic IRISteatotic graftsLiver transplantationAminotransferase levelsCommon indicationNonalcoholic steatohepatitisOrgan failure
2016
Lymphoid Aggregates Remodel Lymphatic Collecting Vessels that Serve Mesenteric Lymph Nodes in Crohn Disease
Randolph GJ, Bala S, Rahier JF, Johnson MW, Wang PL, Nalbantoglu I, Dubuquoy L, Chau A, Pariente B, Kartheuser A, Zinselmeyer BH, Colombel JF. Lymphoid Aggregates Remodel Lymphatic Collecting Vessels that Serve Mesenteric Lymph Nodes in Crohn Disease. American Journal Of Pathology 2016, 186: 3066-3073. PMID: 27746181, PMCID: PMC5225286, DOI: 10.1016/j.ajpath.2016.07.026.Peer-Reviewed Original ResearchConceptsTertiary lymphoid organsMesenteric lymph nodesLymph nodesCrohn's diseaseLymphatic collecting vesselsInfection-induced tissue damageInnate lymphoid cellsChronic inflammatory stateImmune cell accessHuman intestinal diseasesMesenteric adipose tissueEarly pathological descriptionsAppropriate immunityInflammatory stateLymphoid organsPoor healingIntestinal diseaseLymphoid cellsPathological descriptionAdipose tissueB cellsAnatomical relationshipTissue damageCD specimensLymphatic remodelingCharacterization of Colorectal Cancer Development in Apcmin/+ Mice
Nalbantoglu I, Blanc V, Davidson NO. Characterization of Colorectal Cancer Development in Apcmin/+ Mice. Methods In Molecular Biology 2016, 1422: 309-327. PMID: 27246043, PMCID: PMC5061497, DOI: 10.1007/978-1-4939-3603-8_27.ChaptersConceptsDextran sulfate sodiumCancer developmentCommon pathologic lesionsBile acid supplementationExperimental colorectal cancerColorectal cancer developmentHigh-fat dietColon cancer developmentSulfate sodiumColorectal cancerFat dietAcid supplementationPathologic lesionsTherapeutic aspectsIntestinal neoplasiaC57BL/6J backgroundEnvironmental modifiersExperimental modelMiceExcellent experimental modelTissue processingNeoplasiaLesionsCancer
2014
Intestinal Epithelial HuR Modulates Distinct Pathways of Proliferation and Apoptosis and Attenuates Small Intestinal and Colonic Tumor Development
Giammanco A, Blanc V, Montenegro G, Klos C, Xie Y, Kennedy S, Luo J, Chang SH, Hla T, Nalbantoglu I, Dharmarajan S, Davidson NO. Intestinal Epithelial HuR Modulates Distinct Pathways of Proliferation and Apoptosis and Attenuates Small Intestinal and Colonic Tumor Development. Cancer Research 2014, 74: 5322-5335. PMID: 25085247, PMCID: PMC4167566, DOI: 10.1158/0008-5472.can-14-0726.Peer-Reviewed Original ResearchConceptsTumor burdenSmall intestineFecal bile acid excretionAcute intestinal injuryColitis-associated cancerBile acid excretionBile acid metabolismColonic epithelial cellsAOM-DSSIntestinal deletionIntestinal injuryProapoptotic gene expressionIntestinal cancerCarcinogenesis protocolIntestinal expressionAcid excretionASBT expressionIntestinal tumorigenesisIntestinal growthVillus heightTransgenic modelGenetic deletionMiceExpression of transcriptsHuR gene
2013
Liver Fatty Acid-Binding Protein (L-Fabp) Modifies Intestinal Fatty Acid Composition and Adenoma Formation in ApcMin/+ Mice
Dharmarajan S, Newberry EP, Montenegro G, Nalbantoglu I, Davis VR, Clanahan MJ, Blanc V, Xie Y, Luo J, Fleshman JW, Kennedy S, Davidson NO. Liver Fatty Acid-Binding Protein (L-Fabp) Modifies Intestinal Fatty Acid Composition and Adenoma Formation in ApcMin/+ Mice. Cancer Prevention Research 2013, 6: 1026-1037. PMID: 23921281, PMCID: PMC3791217, DOI: 10.1158/1940-6207.capr-13-0120.Peer-Reviewed Original ResearchMeSH KeywordsAdenomaAnimalsCell ProliferationDietary FatsDinoprostoneFatty Acid-Binding ProteinsFatty AcidsFemaleGene DeletionGene Expression Regulation, NeoplasticGenotypeImmunohistochemistryIntestinal MucosaLipidsMiceMice, TransgenicPolymerase Chain ReactionRNA, MessengerSignal TransductionTime FactorsConceptsFatty acid traffickingDietary fat intakeFatty acid speciesFatty acid-binding proteinAcid-binding proteinFatty acid metabolismFat intakeIntestinal fatty acid metabolismIntestinal tumorigenesisCellular proliferationAcid metabolismFatty acid elongationNuclear hormone receptorsΒ-catenin translocationNuclear β-catenin translocationDiet-induced obesityHigh-grade dysplasiaLiver fatty acid-binding proteinIntestinal fatty acid-binding proteinIntestinal tumor formationImportant genetic modifiersSignificant reductionAcid speciesMetabolic compartmentalizationGenetic modifiersIntestine-Specific Mttp Deletion Increases the Severity of Experimental Colitis and Leads to Greater Tumor Burden in a Model of Colitis Associated Cancer
Xie Y, Matsumoto H, Nalbantoglu I, Kerr TA, Luo J, Rubin DC, Kennedy S, Davidson NO. Intestine-Specific Mttp Deletion Increases the Severity of Experimental Colitis and Leads to Greater Tumor Burden in a Model of Colitis Associated Cancer. PLOS ONE 2013, 8: e67819. PMID: 23805328, PMCID: PMC3689718, DOI: 10.1371/journal.pone.0067819.Peer-Reviewed Original ResearchConceptsMttp-IKO miceDextran sodium sulfateDSS treatmentExperimental colitisTumor burdenColitis-Associated CancerDevelopment of colitisIndependent risk factorDietary fat intakeColonic mRNA expressionLevels of TNFαColonic tumor burdenIntestine-specific deletionMicrosomal triglyceride transfer proteinDSS administrationColonic inflammationColonic injuryIL-17AInflammasome expressionSystemic injuryFat intakeFat malabsorptionColorectal cancerCytokine expressionIL-1β
2012
Transient Inability to Manage Proteobacteria Promotes Chronic Gut Inflammation in TLR5-Deficient Mice
Carvalho FA, Koren O, Goodrich JK, Johansson ME, Nalbantoglu I, Aitken JD, Su Y, Chassaing B, Walters WA, González A, Clemente JC, Cullender TC, Barnich N, Darfeuille-Michaud A, Vijay-Kumar M, Knight R, Ley RE, Gewirtz AT. Transient Inability to Manage Proteobacteria Promotes Chronic Gut Inflammation in TLR5-Deficient Mice. Cell Host & Microbe 2012, 12: 139-152. PMID: 22863420, PMCID: PMC4310462, DOI: 10.1016/j.chom.2012.07.004.Peer-Reviewed Original ResearchConceptsChronic colitisGenetic influencing factorsTLR5-deficient miceChronic gut inflammationLow-grade inflammationMucosal immune systemInnate immune deficiencyProinflammatory gene expressionWild-type miceContribution of microbiotaTransient high levelsGut inflammationImmune deficiencyIntestinal microbiotaColitisGut microbiotaImmune systemMice displayUnstable microbiotaGut epitheliumTransient inabilityMicrobiotaInflammationBreakdown of homeostasisIncomplete penetranceCytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges
Carvalho F, Nalbantoglu I, Aitken J, Uchiyama R, Su Y, Doho G, Vijay-Kumar M, Gewirtz A. Cytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges. Mucosal Immunology 2012, 5: 288-298. PMID: 22318495, PMCID: PMC3328601, DOI: 10.1038/mi.2012.8.Peer-Reviewed Original ResearchConceptsInflammasome activation resultsDevelopment of colitisDextran sulfate sodiumInnate immune activatorsDetection of flagellinIntestinal gene expressionPredispose miceSulfate sodiumEpithelial injuryIL-18IL-1βImmune activatorsIntestinal homeostasisSevere diseaseFlagellin administrationSalmonella infectionMonoclonal antibodiesSystemic challengesMiceNLRC4Transcription-independent pathwayIntestinal genesAdministrationActivation resultsBacterial flagellin
2011
Interleukin-1β (IL-1β) promotes susceptibility of Toll-like receptor 5 (TLR5) deficient mice to colitis
Carvalho FA, Nalbantoglu I, Ortega-Fernandez S, Aitken JD, Su Y, Koren O, Walters WA, Knight R, Ley RE, Vijay-Kumar M, Gewirtz AT. Interleukin-1β (IL-1β) promotes susceptibility of Toll-like receptor 5 (TLR5) deficient mice to colitis. Gut 2011, 61: 373. PMID: 21646247, DOI: 10.1136/gut.2011.240556.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalCecumColitis, UlcerativeDisease Models, AnimalDisease SusceptibilityGene Expression ProfilingInterleukin-1betaMaleMetagenomeMiceMice, KnockoutMyeloid Differentiation Factor 88Receptors, Interleukin-10Reverse Transcriptase Polymerase Chain ReactionSignal TransductionToll-Like Receptor 5ConceptsToll-like receptor 4T5KO miceGut microbiotaColitis modelIL-1βAbsence of TLR4Toll-like receptor 5 deficient (T5KO) miceAnti-inflammatory cytokine interleukin-10Endogenous anti-inflammatory pathwayToll-like receptor 5Loss of TLR5Anti-inflammatory pathwayIL-10 receptorCytokine interleukin-10Double knockoutIL-10 signalingIL-1 receptorProinflammatory gene expressionWild-type littermatesColitogenic microbiotaSpontaneous colitisUniform colitisSevere colitisImmune dysregulationIntestinal inflammation
2009
Tumor Regression following DNA Vaccination and Regulatory T Cell Depletion in neu Transgenic Mice Leads to an Increased Risk for Autoimmunity
Jacob JB, Kong YC, Nalbantoglu I, Snower DP, Wei WZ. Tumor Regression following DNA Vaccination and Regulatory T Cell Depletion in neu Transgenic Mice Leads to an Increased Risk for Autoimmunity. The Journal Of Immunology 2009, 182: 5873-5881. PMID: 19380836, PMCID: PMC3833444, DOI: 10.4049/jimmunol.0804074.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCancer VaccinesCell Line, TumorFemaleGenetic Predisposition to DiseaseLymphocyte DepletionMammary Neoplasms, ExperimentalMiceMice, Inbred BALB CMice, TransgenicNIH 3T3 CellsRatsReceptor, ErbB-2Remission InductionThyroglobulinThyroiditis, AutoimmuneT-Lymphocytes, RegulatoryVaccines, DNAConceptsRegulatory T-cell depletionT-cell depletionDNA vaccinationTumor regressionTreg depletionCell depletionBALB/c miceAnti-tumor immunityNeu transgenic miceAutoimmune manifestationsImmunotherapeutic regimensAutoimmune thyroiditisTolerant miceMouse thyroglobulinTumor immunityCD25 mAbComplete regressionImmune reactivityAutoimmune diseasesC miceCancer immunotherapyCancer patientsClinical trialsFemale miceLong-term protection