2023
Adiponectin in the mammalian host influences ticks’ acquisition of the Lyme disease pathogen Borrelia
Tang X, Cao Y, Booth C, Arora G, Cui Y, Matias J, Fikrig E. Adiponectin in the mammalian host influences ticks’ acquisition of the Lyme disease pathogen Borrelia. PLOS Biology 2023, 21: e3002331. PMID: 37862360, PMCID: PMC10619873, DOI: 10.1371/journal.pbio.3002331.Peer-Reviewed Original ResearchConceptsAdipocyte-derived hormoneBite siteAdiponectin-deficient miceInfiltration of neutrophilsTick bite sitePro-inflammatory responseWild-type animalsIxodes scapularis ticksIL-1βVascular leakageHistamine releaseTick biteAdiponectinInfectious diseasesLyme disease agentBlood feeding arthropodsBorrelia burgdorferiScapularis ticksAnimal infectious diseasesBlood feedingB. burgdorferi survivalHuman bloodHormonePathogen acquisitionMammalian hostsHepatocyte CYR61 polarizes profibrotic macrophages to orchestrate NASH fibrosis
Mooring M, Yeung G, Luukkonen P, Liu S, Akbar M, Zhang G, Balogun O, Yu X, Mo R, Nejak-Bowen K, Poyurovsky M, Booth C, Konnikova L, Shulman G, Yimlamai D. Hepatocyte CYR61 polarizes profibrotic macrophages to orchestrate NASH fibrosis. Science Translational Medicine 2023, 15: eade3157. PMID: 37756381, PMCID: PMC10874639, DOI: 10.1126/scitranslmed.ade3157.Peer-Reviewed Original ResearchConceptsNonalcoholic steatohepatitisLiver inflammationNonalcoholic fatty liver diseaseProgression of NASHCysteine-rich angiogenic inducer 61Fatty liver diseaseLiver-specific knockout miceImproved glucose toleranceType 2 diabetesGlucose toleranceLiver diseaseNASH progressionProfibrotic macrophagesProinflammatory propertiesReduced fibrosisCardiovascular diseaseProfibrotic phenotypeFibrotic developmentKnockout miceNF-κBMetabolic diseasesNASH dietPDGFB expressionFibrosisProfibrotic programPolyvalent mRNA vaccination elicited potent immune response to monkeypox virus surface antigens
Fang Z, Monteiro V, Renauer P, Shang X, Suzuki K, Ling X, Bai M, Xiang Y, Levchenko A, Booth C, Lucas C, Chen S. Polyvalent mRNA vaccination elicited potent immune response to monkeypox virus surface antigens. Cell Research 2023, 33: 407-410. PMID: 36879038, PMCID: PMC9988199, DOI: 10.1038/s41422-023-00792-5.Peer-Reviewed Original ResearchRepeated Tick Infestations Impair Borrelia burgdorferi Transmission in a Non-Human Primate Model of Tick Feeding
Narasimhan S, Booth C, Philipp M, Fikrig E, Embers M. Repeated Tick Infestations Impair Borrelia burgdorferi Transmission in a Non-Human Primate Model of Tick Feeding. Pathogens 2023, 12: 132. PMID: 36678479, PMCID: PMC9861725, DOI: 10.3390/pathogens12010132.Peer-Reviewed Original ResearchNon-human primatesImmune responseLyme diseaseTick transmissionAnimal modelsGuinea pigsNon-human primate modelProtective immune responseTick feedingTick infestationRobust immune responseTick salivary antigensElicit immune responsesHuman Lyme diseaseClinical manifestationsHuman pathogensPrimate modelSalivary antigensNon-natural hostsVaccine targetsDiseaseVaccine discoveryTick resistanceBorreliaNatural host
2022
A microbial transporter of the dietary antioxidant ergothioneine
Dumitrescu D, Gordon E, Kovalyova Y, Seminara A, Duncan-Lowey B, Forster E, Zhou W, Booth C, Shen A, Kranzusch P, Hatzios S. A microbial transporter of the dietary antioxidant ergothioneine. Cell 2022, 185: 4526-4540.e18. PMID: 36347253, PMCID: PMC9691600, DOI: 10.1016/j.cell.2022.10.008.Peer-Reviewed Original ResearchConceptsInter-kingdom competitionHost-associated microbesIntracellular redox homeostasisGastric pathogen Helicobacter pyloriPathogen Helicobacter pyloriRedox regulationSmall molecule antioxidantsRedox homeostasisBiosynthetic pathwayColonization advantageUnappreciated mechanismLMW thiolsHost environmentHuman faecal bacteriaWeight thiolsCertain microorganismsAntioxidant ergothioneineGastrointestinal microbesMetabolite trimethylamine N-oxideMicrobesMillimolar levelsHuman tissuesErgothioneineTrimethylamine N-oxideFecal bacteria
2021
KDM5B promotes immune evasion by recruiting SETDB1 to silence retroelements
Zhang SM, Cai WL, Liu X, Thakral D, Luo J, Chan LH, McGeary MK, Song E, Blenman KRM, Micevic G, Jessel S, Zhang Y, Yin M, Booth CJ, Jilaveanu LB, Damsky W, Sznol M, Kluger HM, Iwasaki A, Bosenberg MW, Yan Q. KDM5B promotes immune evasion by recruiting SETDB1 to silence retroelements. Nature 2021, 598: 682-687. PMID: 34671158, PMCID: PMC8555464, DOI: 10.1038/s41586-021-03994-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorDNA-Binding ProteinsEpigenesis, GeneticGene SilencingHeterochromatinHistone-Lysine N-MethyltransferaseHumansInterferon Type IJumonji Domain-Containing Histone DemethylasesMaleMelanomaMiceMice, Inbred C57BLMice, KnockoutNuclear ProteinsRepressor ProteinsRetroelementsTumor EscapeConceptsImmune checkpoint blockadeImmune evasionCheckpoint blockadeImmune responseAnti-tumor immune responseRobust adaptive immune responseTumor immune evasionAnti-tumor immunityAdaptive immune responsesType I interferon responseDNA-sensing pathwayMouse melanoma modelImmunotherapy resistanceMost patientsCurrent immunotherapiesTumor immunogenicityImmune memoryMelanoma modelCytosolic RNA sensingRole of KDM5BConsiderable efficacyInterferon responseImmunotherapyEpigenetic therapyBlockadeKetogenic diet restrains aging-induced exacerbation of coronavirus infection in mice
Ryu S, Shchukina I, Youm YH, Qing H, Hilliard B, Dlugos T, Zhang X, Yasumoto Y, Booth CJ, Fernández-Hernando C, Suárez Y, Khanna K, Horvath TL, Dietrich MO, Artyomov M, Wang A, Dixit VD. Ketogenic diet restrains aging-induced exacerbation of coronavirus infection in mice. ELife 2021, 10: e66522. PMID: 34151773, PMCID: PMC8245129, DOI: 10.7554/elife.66522.Peer-Reviewed Original ResearchConceptsΓδ T cellsKetogenic dietCoronavirus infectionAged miceT cellsHigher systemic inflammationInfected aged miceCOVID-19 severityCOVID-19 infectionActivation of ketogenesisMouse hepatitis virus strain A59Systemic inflammationInflammatory damageInfluenza infectionClinical hallmarkNLRP3 inflammasomeImmune surveillanceAdipose tissuePotential treatmentInfectionMiceStrongest predictorLungMortalityAgeDeletion of Cdh16 Ksp-cadherin leads to a developmental delay in the ability to maximally concentrate urine in mouse
Thomson R, Dynia DW, Burlein S, Thomson BR, Booth C, Knauf F, Wang T, Aronson P. Deletion of Cdh16 Ksp-cadherin leads to a developmental delay in the ability to maximally concentrate urine in mouse. American Journal Of Physiology. Renal Physiology 2021, 320: f1106-f1122. PMID: 33938239, PMCID: PMC8285649, DOI: 10.1152/ajprenal.00556.2020.Peer-Reviewed Original ResearchConceptsKsp-cadherinCell adhesion moleculeAtypical memberKidney developmentMammalian kidneyAdult mammalian kidneyBasolateral membraneNormal kidney developmentEpithelial cellsAdhesion moleculesMutant animalsExpression analysisSpecific expressionE-cadherin expressionWestern blot analysisEpithelial phenotypePrincipal proteinE-cadherinBlot analysisMouse linesAquaporin-2CadherinCritical roleDevelopmental delayKnockout mice
2017
PEGylated PLGA Nanoparticles for the Improved Delivery of Doxorubicin
Park J, Fong P, Lu J, Russell K, Booth C, Mark Saltzman W, Fahmy T. PEGylated PLGA Nanoparticles for the Improved Delivery of Doxorubicin. 2017, 575-596. DOI: 10.1201/b22358-23.Peer-Reviewed Original ResearchPEGylated PLGA Nanoparticles for the Improved Delivery of Doxorubicin
Park J, Fong P, Lu J, Russell K, Booth C, Saltzman W, Fahmy T. PEGylated PLGA Nanoparticles for the Improved Delivery of Doxorubicin. 2017, 575-596. DOI: 10.1201/9781315114361-23.Peer-Reviewed Original Research
2015
Employing a Gain-of-Function Factor IX Variant R338L to Advance the Efficacy and Safety of Hemophilia B Human Gene Therapy: Preclinical Evaluation Supporting an Ongoing Adeno-Associated Virus Clinical Trial
Monahan PE, Sun J, Gui T, Hu G, Hannah WB, Wichlan DG, Wu Z, Grieger JC, Li C, Suwanmanee T, Stafford DW, Booth CJ, Samulski JJ, Kafri T, McPhee SW, Samulski RJ. Employing a Gain-of-Function Factor IX Variant R338L to Advance the Efficacy and Safety of Hemophilia B Human Gene Therapy: Preclinical Evaluation Supporting an Ongoing Adeno-Associated Virus Clinical Trial. Human Gene Therapy 2015, 26: 69-81. PMID: 25419787, PMCID: PMC4326268, DOI: 10.1089/hum.2014.106.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, NeutralizingCapsidClinical Trials as TopicDependovirusDisease Models, AnimalDrug Evaluation, PreclinicalFactor IXGene ExpressionGenetic EngineeringGenetic TherapyGenetic VectorsHemophilia BHemorrhageHumansLiverMaleMiceMice, Inbred C57BLMice, KnockoutRecombinant ProteinsTailTissue DistributionVirionConceptsHuman clinical trialsClinical trialsVector deliveryDose-dependent inflammationAbility of adenoLiver infiltratesMacrovascular thrombosisHemophilic arthropathyClinical morbidityHistopathological findingsMice 8Mild hemophilia BHemophilic miceEfficacy profileNormal micePreclinical studiesIdentical dosesMarked tropismPreclinical evaluationClinical successFIX antibodyTail transectionFIX activityBiodistribution evaluationFunction variants
2014
Proteomics Identify Haptoglobin as a Novel Enhancer of Cardiac Transplant Rejection.
Goldstein D, Heuzey E, Mori D, Colangelo C, Chung L, Bruce C, Booth C, Kreisel D, Shen H. Proteomics Identify Haptoglobin as a Novel Enhancer of Cardiac Transplant Rejection. Transplantation 2014, 98: 885. DOI: 10.1097/00007890-201407151-03021.Peer-Reviewed Original Research(432) Discovering Novel Inflammatory Triggers after Heart Transplantation Via Proteomics
Shen H, Colangelo C, Chung L, Bruce C, Booth C, Kreisel D, Goldstein D. (432) Discovering Novel Inflammatory Triggers after Heart Transplantation Via Proteomics. The Journal Of Heart And Lung Transplantation 2014, 33: s164. DOI: 10.1016/j.healun.2014.01.439.Peer-Reviewed Original Research
2013
Activation Induced Cytidine Deaminase-Associated DNA Repair Pathways Influence Germinal Center B Cell Lymphomagenesis
Gu X, Booth C, Liu Z, Strout M. Activation Induced Cytidine Deaminase-Associated DNA Repair Pathways Influence Germinal Center B Cell Lymphomagenesis. Blood 2013, 122: 1247. DOI: 10.1182/blood.v122.21.1247.1247.Peer-Reviewed Original ResearchDiffuse large B-cell lymphomaB-cell lymphomaMsh2-/- miceCell lymphomaB cellsChromosome abnormalitiesLarge B-cell lymphomaShorter median timePre-B-cell tumorsSquamous cell carcinomaFollicular B-cell lymphomaT-cell lymphomaHuman diffuse large B-cell lymphomaGerminal center B cellsMSH2-dependent mismatch repairPathogenesis of GCSingle-deficient miceDevelopment of DLBCLNet protective effectDevelopment of tumorsClonal mutationsPre-B cell lymphomaGC B cellsMedian survivalMedian time
2011
Corrections: Viral Infection of the Placenta Leads to Fetal Inflammation and Sensitization to Bacterial Products Predisposing to Preterm Labor
Cardenas I, Means R, Aldo P, Koga K, Lang S, Booth C, Manzur A, Oyarzun E, Romero R, Mor G. Corrections: Viral Infection of the Placenta Leads to Fetal Inflammation and Sensitization to Bacterial Products Predisposing to Preterm Labor. The Journal Of Immunology 2011, 187: 2835-2835. DOI: 10.4049/jimmunol.1190048.Peer-Reviewed Original Research
2010
Viral Infection of the Placenta Leads to Fetal Inflammation and Sensitization to Bacterial Products Predisposing to Preterm Labor
Cardenas I, Means RE, Aldo P, Koga K, Lang SM, Booth C, Manzur A, Oyarzun E, Romero R, Mor G. Viral Infection of the Placenta Leads to Fetal Inflammation and Sensitization to Bacterial Products Predisposing to Preterm Labor. The Journal Of Immunology 2010, 185: 1248-1257. PMID: 20554966, PMCID: PMC3041595, DOI: 10.4049/jimmunol.1000289.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBacterial InfectionsCell LineCells, CulturedCytokinesFemaleFetal DiseasesFetusHost-Pathogen InteractionsHumansImmunohistochemistryInflammationMaternal-Fetal ExchangeMiceMice, Inbred C57BLMice, KnockoutNIH 3T3 CellsObstetric Labor, PrematurePlacentaPlacenta DiseasesPregnancyPregnancy Complications, InfectiousRhadinovirusToll-Like Receptor 3Virus DiseasesConceptsViral infectionPreterm laborBacterial productsFetal inflammatory responseMaternal immune systemFetal transmissionFetal inflammationNonpregnant populationOrgan damagePregnant womenPregnant mothersPlacental unitInflammatory responseImmunological roleAnimal modelsImmune systemInfectionPlacentaMicrobial infectionsFetusesDevelopmental deficienciesMothersDetrimental effectsPandemicInflammation
2009
Evaluation of hepatic fibrosis with portal pressure gradient in rats
Wang Y, Booth CJ, Kim H, Qiu M, Constable RT. Evaluation of hepatic fibrosis with portal pressure gradient in rats. Magnetic Resonance In Medicine 2009, 61: 1185-1192. PMID: 19253377, PMCID: PMC11210607, DOI: 10.1002/mrm.21964.Peer-Reviewed Original ResearchConceptsHepatic fibrosisFibrosis scorePortal pressure gradientCirrhosis groupFibrosis groupLiver fibrosisLiver pathologyPortal veinHistological examinationAnimal studiesNoninvasive assessmentFibrosisNoninvasive meansGradient echo sequenceVessel areaSignificant differencesRatsContrast agentsEcho sequenceScoresCarbon tetrachlorideGroupPhantom study
2008
Induced Hepatic Fibrosis in Rats: Hepatic Steatosis, Macromolecule Content, Perfusion Parameters, and Their Correlations—Preliminary MR Imaging in Rats
Kim H, Booth CJ, Pinus AB, Chen P, Lee A, Qiu M, Whitlock M, Murphy PS, Constable RT. Induced Hepatic Fibrosis in Rats: Hepatic Steatosis, Macromolecule Content, Perfusion Parameters, and Their Correlations—Preliminary MR Imaging in Rats. Radiology 2008, 247: 696-705. PMID: 18403622, DOI: 10.1148/radiol.2473070605.Peer-Reviewed Original Research
2007
Fetal nucleated red blood cells in a rat model of intrauterine growth restriction induced by hypoxia and nitric oxide synthase inhibition
Ravishankar V, Buhimschi CS, Booth CJ, Bhandari V, Norwitz E, Copel J, Buhimschi IA. Fetal nucleated red blood cells in a rat model of intrauterine growth restriction induced by hypoxia and nitric oxide synthase inhibition. American Journal Of Obstetrics And Gynecology 2007, 196: 482.e1-482.e8. PMID: 17466713, DOI: 10.1016/j.ajog.2006.12.020.Peer-Reviewed Original ResearchConceptsIntrauterine growth restrictionNucleated red blood cellsNitric oxide inhibitionFetal nucleated red blood cellsChronic hypoxiaL-NAMEErythropoietin levelsOxide inhibitionRed blood cellsFetal circulationGrowth restrictionFetal bloodHematocrit levelsNumber of NRBCsNitro-L-arginine methyl esterChronic nitric oxide inhibitionMaternal acid-base statusNitric oxide synthase inhibitionBlood cellsMaternal arterial blood gasesOxide synthase inhibitionArterial blood gasesSaline solutionAdult Sprague-DawleyElevated erythropoietin levels
2006
Attenuation of signaling pathways stimulated by pathologically activated FGF-receptor 2 mutants prevents craniosynostosis
Eswarakumar VP, Özcan F, Lew ED, Bae JH, Tomé F, Booth CJ, Adams DJ, Lax I, Schlessinger J. Attenuation of signaling pathways stimulated by pathologically activated FGF-receptor 2 mutants prevents craniosynostosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2006, 103: 18603-18608. PMID: 17132737, PMCID: PMC1693709, DOI: 10.1073/pnas.0609157103.Peer-Reviewed Original ResearchConceptsFGF receptorsDocking protein FRS2alphaCommon craniofacial abnormalitySelective uncouplingPremature fusionSkull developmentFunction mutationsDominant mutationsNormal skull developmentMurine model systemMutationsSevere bone disordersModel systemFGFR2cCraniofacial abnormalitiesCalvaria organ culturesPathwayOrgan cultureFRS2alphaSkull vaultMutantsPharmacological approachesFusionFGFRUncoupling