2024
Dual roles for a tick protein disulfide isomerase during the life cycle of the Lyme disease agent
Tang X, Cui Y, Namarra U, Tian X, Rivas-Giorgi F, Fikrig E. Dual roles for a tick protein disulfide isomerase during the life cycle of the Lyme disease agent. MBio 2024, 15: e01754-24. PMID: 39470213, PMCID: PMC11633212, DOI: 10.1128/mbio.01754-24.Peer-Reviewed Original ResearchProtein disulfide isomeraseLyme disease agentDisulfide isomeraseBlood-feeding vectorsExtracellular pathogensGene expressionInvasion of host cellsThiol-disulfide oxidoreductasesDisease agentsGroup of enzymesStages of bacterial infectionVirulence factorsLife cycleChaperone activityMammalian hostsHost cellsBlood-feeding ticksIsomeraseMicrobial infectionsColonized ticksPathogensDiverse infectionsMicrobial invasionInfection of miceVector-borne diseasesTargeting Pseudomonas aeruginosa biofilm with an evolutionary trained bacteriophage cocktail exploiting phage resistance trade-offs
Kunisch F, Campobasso C, Wagemans J, Yildirim S, Chan B, Schaudinn C, Lavigne R, Turner P, Raschke M, Trampuz A, Gonzalez Moreno M. Targeting Pseudomonas aeruginosa biofilm with an evolutionary trained bacteriophage cocktail exploiting phage resistance trade-offs. Nature Communications 2024, 15: 8572. PMID: 39362854, PMCID: PMC11450229, DOI: 10.1038/s41467-024-52595-w.Peer-Reviewed Original ResearchConceptsResistance trade-offBacteriophage host rangeViruses of bacteriaHuman microbial infectionsMultidrug-resistant bacterial infectionsTwo-phage cocktailMultidrug-resistant Pseudomonas aeruginosa strainsLytic bacteriophagesBiofilm-associatedEvolution assaysPlanktonic culturesBacteriophage cocktailHost rangeBacteriophageHost spectrumBacteriophage therapyCocktail designCombat biofilmsTreated bacteriaMicrobial infectionsAntimicrobial efficacyBacterial suppressionPolymerase chain reactionBacterial infectionsClinical outcomesA cluster of type I interferon-regulated genes associates with disease activity and prognosis in patients with IgA nephropathy
Qu S, Gan T, Wang Y, Qi Y, Zhang Y, Berthier C, Liu L, Shi S, Lv J, Zhang H, Zhou X. A cluster of type I interferon-regulated genes associates with disease activity and prognosis in patients with IgA nephropathy. International Immunopharmacology 2024, 131: 111920. PMID: 38522142, DOI: 10.1016/j.intimp.2024.111920.Peer-Reviewed Original ResearchIFN-regulated genesIFN-scoreIgAN patientsIgA nephropathyIFN-ITubular atrophy/interstitial fibrosisHigher IFN levelsCox regression analysisPathogenesis of IgA nephropathyType I interferonCross-sectional studyGross hematuriaMucosal infectionsRenal outcomesDisease activityIFN scoreInduce high levelsIFN levelsHealthy controlsMesangial hypercellularityIgANI interferonPatientsTherapeutic targetMicrobial infections
2023
Posttransplant Tertiary Lymphoid Organs
Ruddle N. Posttransplant Tertiary Lymphoid Organs. Transplantation 2023, 108: 1090-1099. PMID: 37917987, PMCID: PMC11042531, DOI: 10.1097/tp.0000000000004812.Peer-Reviewed Original ResearchTertiary lymphoid organsOrgan rejectionLymphoid organsCase of immunosuppressionEctopic lymphoid structuresDevelopment of lymphomaLymphoid neogenesisLymph nodesIschemic reperfusionChronic inflammationLymphoid structuresNephrotoxic agentsTumor antigensVascular componentLymphoid cellsTherapeutic manipulationSustained exposureMicrobial infectionsCellular compositionStaging schemeCancerOrgansRejectionImmunosuppressionReperfusion
2022
Inflammatory stress signaling via NF-kB alters accessible cholesterol to upregulate SREBP2 transcriptional activity in endothelial cells
Fowler JWM, Zhang R, Tao B, Boutagy NE, Sessa WC. Inflammatory stress signaling via NF-kB alters accessible cholesterol to upregulate SREBP2 transcriptional activity in endothelial cells. ELife 2022, 11: e79529. PMID: 35959888, PMCID: PMC9395194, DOI: 10.7554/elife.79529.Peer-Reviewed Original ResearchConceptsAcute inflammatory responseEndothelial cellsCholesterol homeostasisInflammatory stressInflammatory responsePro-inflammatory cytokinesSite of injuryCholesterol biosynthetic gene expressionNF-κB DNA bindingHuman endothelial cellsMultiple sclerosisInflammatory activationPrimary human endothelial cellsVascular endotheliumNF-κB-inducible genesTissue damageInducible targetAberrant activationRole of cholesterolSREBP2 activationMicrobial infectionsCholesterolKey transcription regulatorHomeostasisLeukocytesTuft cells are key mediators of interkingdom interactions at mucosal barrier surfaces
Strine MS, Wilen CB. Tuft cells are key mediators of interkingdom interactions at mucosal barrier surfaces. PLOS Pathogens 2022, 18: e1010318. PMID: 35271673, PMCID: PMC8912186, DOI: 10.1371/journal.ppat.1010318.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsInterkingdom interactionsTuft cellsCell biologyImmune responseMicrobial activationMicrobial sensingCell abundanceMucosal barrier surfacesAntiviral adaptive immune responsesType 2 immune responsesCell heterogeneityExquisite specificityMucosal barrier integrityAdaptive immune responsesMurine norovirusHuman healthKey orchestratorsMicrobial infectionsPathogenic bacteriaBroad intraFlavivirus replicationKey mediatorContext of coinfectionTissue repairImmune evasion
2019
Introduction to Immunology, Epidemiology, and Immunoepidemiology
Niccolai L, Ruddle N, Krause P. Introduction to Immunology, Epidemiology, and Immunoepidemiology. 2019, 3-17. DOI: 10.1007/978-3-030-25553-4_1.ChaptersIndividual multicellular organismsImmune responseMulticellular organismsRelevant health problemHealth-related eventsInflammatory diseasesSelect populationCombination of cellsHealth problemsEpidemiologic toolImmunoepidemiologyMicrobial infectionsEpidemiologyGenetic polymorphismsImmunologyEnvironmental factorsPopulationAutoimmunityMalignancyOrganismsInfectionDiversityDiseaseStudyModelling microbial infection to address global health challenges
Fitzpatrick MC, Bauch CT, Townsend JP, Galvani AP. Modelling microbial infection to address global health challenges. Nature Microbiology 2019, 4: 1612-1619. PMID: 31541212, PMCID: PMC6800015, DOI: 10.1038/s41564-019-0565-8.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsOptimization of modelsGlobal health challengeDisease transmission dynamicsHealth challengesEpidemiological modellingAccuracy of predictionDifferent intervention strategiesPandemic preparednessInfectious diseasesTransmission dynamicsMicrobial infectionsIntervention strategiesModel developmentPublic healthDiseaseHIV crisisModelOptimizationRiskHealthDynamicsModellingClose collaborationMethodological advancesModelersBright Green Biofluorescence in Sharks Derives from Bromo-Kynurenine Metabolism
Park HB, Lam YC, Gaffney JP, Weaver JC, Krivoshik SR, Hamchand R, Pieribone V, Gruber DF, Crawford JM. Bright Green Biofluorescence in Sharks Derives from Bromo-Kynurenine Metabolism. IScience 2019, 19: 1291-1336. PMID: 31402257, PMCID: PMC6831821, DOI: 10.1016/j.isci.2019.07.019.Peer-Reviewed Original ResearchGreen fluorescent proteinGFP-like proteinsSpecies of sharksAcid-binding proteinFluorescence microscopy studiesFatty acid-binding proteinUndescribed groupSmall molecule metabolitesLuminescent phenotypeFluorescent proteinProteinMicrobial infectionsBiofluorescenceMarine environmentSharksSmall moleculesStructural detailsDiscovery of metabolitesWidespread natureCentral nervous systemNervous systemSpectral characterizationSpeciesMetabolitesDiversityGlycerol phosphate shuttle enzyme GPD2 regulates macrophage inflammatory responses
Langston PK, Nambu A, Jung J, Shibata M, Aksoylar HI, Lei J, Xu P, Doan MT, Jiang H, MacArthur MR, Gao X, Kong Y, Chouchani ET, Locasale JW, Snyder NW, Horng T. Glycerol phosphate shuttle enzyme GPD2 regulates macrophage inflammatory responses. Nature Immunology 2019, 20: 1186-1195. PMID: 31384058, PMCID: PMC6707851, DOI: 10.1038/s41590-019-0453-7.Peer-Reviewed Original ResearchConceptsAcetyl coenzyme AGlycerol phosphate shuttleInduction of genesCoenzyme APhosphate shuttleAcetylation of histonesHistone acetylationInflammatory responseMitochondrial glycerolGPD2Inflammatory mediatorsMicrobial infectionsMicrobial stimulationGenesHost defenseGlucose oxidationAcetylationOxidative metabolismBacterial lipopolysaccharideSustained inflammationMacrophage activationHistonesDetrimental effectsMacrophagesAcute exposure
2018
Activity-Based Protein Profiling at the Host–Pathogen Interface
Kovalyova Y, Hatzios SK. Activity-Based Protein Profiling at the Host–Pathogen Interface. Current Topics In Microbiology And Immunology 2018, 420: 73-91. PMID: 30203396, DOI: 10.1007/82_2018_129.BooksConceptsActivity-based protein profilingHost-pathogen interfaceProtein profilingFunctional proteomePathogen interactionsMicrobial pathogenicityComplex proteomesEnzyme-mediated mechanismReactive amino acidsActive enzymeChemical probesAmino acidsMetabolic adaptationProteomeMicrobial infectionsCo-culture systemBiological systemsHost immunityEnzymeProfilingPathogenicityHostProbeAnimal modelsAdaptation
2016
Interleukin-17A Promotes CD8+ T Cell Cytotoxicity To Facilitate West Nile Virus Clearance
Acharya D, Wang P, Paul AM, Dai J, Gate D, Lowery JE, Stokic DS, Leis AA, Flavell RA, Town T, Fikrig E, Bai F. Interleukin-17A Promotes CD8+ T Cell Cytotoxicity To Facilitate West Nile Virus Clearance. Journal Of Virology 2016, 91: 10.1128/jvi.01529-16. PMID: 27795421, PMCID: PMC5165211, DOI: 10.1128/jvi.01529-16.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrainCytotoxicity, ImmunologicFemaleGene ExpressionHumansInterleukin-17MiceMice, Inbred C57BLNeuronsPrimary Cell CultureReceptors, Interleukin-17Recombinant ProteinsSurvival AnalysisT-Lymphocytes, CytotoxicTreatment OutcomeViral LoadVirus ReplicationWest Nile FeverWest Nile virusConceptsT cell cytotoxicityRecombinant IL-17AWest Nile virus infectionWNV-infected miceIL-17AT cellsViral burdenWNV infectionCell cytotoxicityInterleukin-17AVirus infectionMicrobial infectionsIL-17A-deficient miceT cell-mediated clearanceHigh viral burdenT-cell axisLethal WNV infectionSurvival of miceDay 6 postinfectionT cell functionWild-type miceDiverse immune functionsIL-17A.Proinflammatory cytokinesAutoimmune diseasesHigh Endothelial Venules and Lymphatic Vessels in Tertiary Lymphoid Organs: Characteristics, Functions, and Regulation
Ruddle NH. High Endothelial Venules and Lymphatic Vessels in Tertiary Lymphoid Organs: Characteristics, Functions, and Regulation. Frontiers In Immunology 2016, 7: 491. PMID: 27881983, PMCID: PMC5101196, DOI: 10.3389/fimmu.2016.00491.Peer-Reviewed Original ResearchTertiary lymphoid organsHigh endothelial venulesSecondary lymphoid organsLymph nodesAntigen-presenting cellsLymphoid organsEndothelial venulesLymphatic vesselsStromal cellsCentral memory cellsPrimary lymphoid organsTransport antigensGraft rejectionEffector cellsChemokine expressionChronic inflammationPeyer's patchesAntigen presentationInflammatory signalsB cellsBone marrowImmune systemReticular cellsMicrobial infectionsCellular compositionA Family of Salmonella Type III Secretion Effector Proteins Selectively Targets the NF-κB Signaling Pathway to Preserve Host Homeostasis
Sun H, Kamanova J, Lara-Tejero M, Galán JE. A Family of Salmonella Type III Secretion Effector Proteins Selectively Targets the NF-κB Signaling Pathway to Preserve Host Homeostasis. PLOS Pathogens 2016, 12: e1005484. PMID: 26933955, PMCID: PMC4775039, DOI: 10.1371/journal.ppat.1005484.Peer-Reviewed Original ResearchConceptsNF-κBHost homeostasisNF-κB Signaling PathwayHost innate immune responsePro-inflammatory cytokinesInnate immune responseType III secretion effector proteinsHost tissue damageIntestinal inflammationSalmonella typhimurium strainsImmune responseAnimal modelsInflammationRelB transcription factorPathogen replicationMicrobial infectionsTyphimurium strainsEffector proteinsSignaling pathwaysType III secretion systemInfectionBacterial pathogensBacteria Salmonella typhimuriumSignal transduction pathwaysSalmonella typhimuriumTertiary Lymphoid Tissues
Ruddle N. Tertiary Lymphoid Tissues. 2016, 480-485. DOI: 10.1016/b978-0-12-374279-7.07012-0.Peer-Reviewed Original ResearchTertiary lymphoid organsTertiary lymphoid tissueSecondary lymphoid organsLymphoid organsLymphoid tissueConventional lymphoid organsChronic graft rejectionHigh endothelial venulesChronic microbial infectionsStromal cellular compositionAntigen primingNonlymphoid organsGraft rejectionDeterminant spreadingLymph nodesChronic inflammationEndothelial venulesClinical diseaseImmune responseInfectious organismsMicrobial infectionsCellular compositionLymphatic vesselsEctopic sitesAutoimmunity
2014
Unanchored K48-Linked Polyubiquitin Synthesized by the E3-Ubiquitin Ligase TRIM6 Stimulates the Interferon-IKKε Kinase-Mediated Antiviral Response
Rajsbaum R, Versteeg GA, Schmid S, Maestre AM, Belicha-Villanueva A, Martínez-Romero C, Patel JR, Morrison J, Pisanelli G, Miorin L, Laurent-Rolle M, Moulton HM, Stein DA, Fernandez-Sesma A, tenOever BR, García-Sastre A. Unanchored K48-Linked Polyubiquitin Synthesized by the E3-Ubiquitin Ligase TRIM6 Stimulates the Interferon-IKKε Kinase-Mediated Antiviral Response. Immunity 2014, 40: 880-895. PMID: 24882218, PMCID: PMC4114019, DOI: 10.1016/j.immuni.2014.04.018.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntiviral AgentsCells, CulturedEnzyme ActivationHumansI-kappa B KinaseInterferon Type IJanus Kinase 1MicePhosphorylationPolyubiquitinRNA InterferenceRNA, Small InterferingSignal TransductionSTAT1 Transcription FactorTripartite Motif ProteinsUbiquitin-Conjugating EnzymesUbiquitin-Protein LigasesConceptsUnanchored K48Polyubiquitin chainsUnanchored polyubiquitin chainsUpregulation of hundredsAntiviral responseIκB kinase epsilonTripartite motif (TRIM) familyIKKε activationMotif familyKinase activationCellular factorsUBE2KReceptor signalingSTAT1 phosphorylationK48Kinase epsilonType I interferonIFN signalingIFN receptor signalingTRIM6Microbial infectionsISG inductionI interferonSignalingIKKε
2013
Follicular T‐helper cells: controlled localization and cellular interactions
Qi H, Chen X, Chu C, Lu P, Xu H, Yan J. Follicular T‐helper cells: controlled localization and cellular interactions. Immunology And Cell Biology 2013, 92: 28-33. PMID: 24145857, DOI: 10.1038/icb.2013.59.Peer-Reviewed Original ResearchConceptsB cell responsesGerminal centersTfh cellsEffective antibody-based vaccineFollicular T helper cellsDependent B cell responsesIsotype-switched antibodiesAntibody-based vaccinesCD4 T cellsT helper cellsHumoral autoimmunityHumoral protectionT cellsTranscriptional repressor Bcl-6Surface phenotypeSuch antibodiesBCL-6Microbial infectionsGC reactionAntibodiesCellsCellular interactionsCurrent understandingHigh levelsAutoimmunityInflammasomes and Mucosal Immune Response
Elinav E, Henao-Mejia J, Flavell R. Inflammasomes and Mucosal Immune Response. Else Kröner-Fresenius Symposia 2013, 4: 48-52. DOI: 10.1159/000346510.Peer-Reviewed Original ResearchProtein complexesImmune responseDamage signalsCritical regulatorMolecular characterizationContext of infectionInnate immune responseCell deathMucosal immune responsesMicrobial infectionsPotent inflammatory cytokineCaspase-1Direct activationInflammatory cytokinesSterile inflammationMetabolic disordersInflammasome resultsDiverse rangeInflammasomeKey componentRegulatorInfectionProteinNLRC4AIM2
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
2008
Toll‐Like Receptors and Diabetes
Wong F, Wen L. Toll‐Like Receptors and Diabetes. Annals Of The New York Academy Of Sciences 2008, 1150: 123-132. PMID: 19120280, DOI: 10.1196/annals.1447.063.Peer-Reviewed Original ResearchConceptsToll-like receptorsAntigen-presenting cellsType 1 interferonAdaptive immune systemRegulatory cellsAutoimmune responseInflammatory cytokinesMore specific responsesIFN-alphaImmune responseEndogenous ligandImmune systemMolecular patternsInfectionMicrobial infectionsReceptorsInterferonEndogenous stimuliDirect effectCellular stressSpecific responsesCellsResponseAutoimmunityDiabetes
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