2023
Metabolomic changes associated with acquired resistance to Ixodes scapularis
Cui Y, Matias J, Tang X, Cibichakravarthy B, DePonte K, Wu M, Fikrig E. Metabolomic changes associated with acquired resistance to Ixodes scapularis. Ticks And Tick-borne Diseases 2023, 15: 102279. PMID: 37972499, DOI: 10.1016/j.ttbdis.2023.102279.Peer-Reviewed Original ResearchGuinea pigsHydroxyphenyllactic acidMetabolome of serumGroups of miceTyrosine metabolic pathwayTick biteImmune responseControl animalsIxodes scapularisTick salivaI. scapularisMiceInduction of componentsMetabolomic changesMortalityNitisinoneMolecular mechanismsAnimalsMetabolism pathwaysTyrosine degradationPigsTyrosine metabolism pathwayMetabolic pathwaysScapularisMetabolome
2022
A tick C1q protein alters infectivity of the Lyme disease agent by modulating interferon γ
Tang X, Arora G, Matias J, Hart T, Cui Y, Fikrig E. A tick C1q protein alters infectivity of the Lyme disease agent by modulating interferon γ. Cell Reports 2022, 41: 111673. PMID: 36417869, PMCID: PMC9909562, DOI: 10.1016/j.celrep.2022.111673.Peer-Reviewed Original Research
2019
ELF4 facilitates innate host defenses against Plasmodium by activating transcription of Pf4 and Ppbp
Wang D, Zhang Z, Cui S, Zhao Y, Craft S, Fikrig E, You F. ELF4 facilitates innate host defenses against Plasmodium by activating transcription of Pf4 and Ppbp. Journal Of Biological Chemistry 2019, 294: 7787-7796. PMID: 30898878, PMCID: PMC6514618, DOI: 10.1074/jbc.ra118.006321.Peer-Reviewed Original ResearchConceptsPlatelet factor 4Host defenseComponent of plateletsPro-platelet basic proteinKilling of parasitesFactor 4Innate immune moleculesInnate immune signalingInnate host defenseC chemokinesWT littermatesTranscription factor 4Control animalsImmune moleculesInnate immunityInfected erythrocytesImmune signalingInfectionExpression levelsMiceType IBasic proteinDefense peptidesPlateletsPlasmodium
2013
MyD88 Deficiency Markedly Worsens Tissue Inflammation and Bacterial Clearance in Mice Infected with Treponema pallidum, the Agent of Syphilis
Silver AC, Dunne DW, Zeiss CJ, Bockenstedt LK, Radolf JD, Salazar JC, Fikrig E. MyD88 Deficiency Markedly Worsens Tissue Inflammation and Bacterial Clearance in Mice Infected with Treponema pallidum, the Agent of Syphilis. PLOS ONE 2013, 8: e71388. PMID: 23940747, PMCID: PMC3734110, DOI: 10.1371/journal.pone.0071388.Peer-Reviewed Original ResearchConceptsMyD88-deficient miceTreponema pallidumMyD88-deficient animalsResistance of miceToll-like receptorsWild-type miceMyD88-deficient macrophagesMacrophage-mediated clearanceHigh pathogen burdenMyD88 deficiencySpirochete Treponema pallidumWT miceTissue infiltratesBacterial clearanceExtensive inflammationTissue inflammationPlasma cellsControl animalsWT macrophagesMost TLRsAnimal modelsMixed mononuclearPathogen burdenMiceT. pallidum
2008
ICAM-1 Participates in the Entry of West Nile Virus into the Central Nervous System
Dai J, Wang P, Bai F, Town T, Fikrig E. ICAM-1 Participates in the Entry of West Nile Virus into the Central Nervous System. Journal Of Virology 2008, 82: 4164-4168. PMID: 18256150, PMCID: PMC2292986, DOI: 10.1128/jvi.02621-07.Peer-Reviewed Original ResearchConceptsWest Nile virusICAM-1Control animalsWest Nile virus neuroinvasionBlood-brain barrier leakagePathogenesis of encephalitisNile virusBlood-brain barrierLow viral loadWest Nile encephalitisCentral nervous systemICAM-1 participatesVirus neuroinvasionNeuronal damageLeukocyte infiltrationViral encephalitisViral loadBarrier leakageViral infectionNervous systemEncephalitisMiceICAMVirusAnimals
2007
ASC/PYCARD and Caspase-1 Regulate the IL-18/IFN-γ Axis during Anaplasma phagocytophilum Infection
Pedra JH, Sutterwala FS, Sukumaran B, Ogura Y, Qian F, Montgomery RR, Flavell RA, Fikrig E. ASC/PYCARD and Caspase-1 Regulate the IL-18/IFN-γ Axis during Anaplasma phagocytophilum Infection. The Journal Of Immunology 2007, 179: 4783-4791. PMID: 17878377, DOI: 10.4049/jimmunol.179.7.4783.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid MotifsAnaplasmaAnaplasmosisAnimalsApoptosis Regulatory ProteinsCalcium-Binding ProteinsCaspase 1Disease SusceptibilityEnzyme ActivationHL-60 CellsHumansInterferon-gammaInterleukin-18Killer Cells, NaturalMiceMice, Inbred C57BLMice, KnockoutPhagocytosisSignal TransductionTh1 CellsT-Lymphocytes, RegulatoryConceptsA. phagocytophilum infectionIFN-gamma productionCaspase-1Phagocytophilum infectionIFN-gammaA. phagocytophilumIFN-gamma levelsNOD-like receptor pathwayIL-18 secretionIFN-gamma-mediated controlCentral adaptor moleculeAnaplasma phagocytophilum infectionVitro restimulationIL-18Peripheral bloodControl animalsReceptor pathwayASC deficiencyInfectionObligate intracellular pathogensIntracellular pathogensAnaplasma phagocytophilumPhagocytophilumAdaptor moleculeCritical role
2006
Antiviral Peptides Targeting the West Nile Virus Envelope Protein
Bai F, Town T, Pradhan D, Cox J, Ashish, Ledizet M, Anderson JF, Flavell RA, Krueger JK, Koski RA, Fikrig E. Antiviral Peptides Targeting the West Nile Virus Envelope Protein. Journal Of Virology 2006, 81: 2047-2055. PMID: 17151121, PMCID: PMC1797586, DOI: 10.1128/jvi.01840-06.Peer-Reviewed Original ResearchConceptsWest Nile virusMurine blood-brain barrierEnvelope proteinBlood-brain barrierPeptide 9West Nile encephalitisWNV envelope proteinCentral nervous systemWest Nile virus envelope proteinCDNA phage display libraryBrain parenchymaVirus envelope proteinHuman encephalitisViral envelope proteinsWNV infectionControl animalsPeptide-1Nervous systemRelated flavivirusesDengue virusAntiviral activityNew therapeuticsInhibition concentrationAntiviral peptidesNile virus
2004
CXCR2 Blockade Influences Anaplasma phagocytophilum Propagation but Not Histopathology in the Mouse Model of Human Granulocytic Anaplasmosis
Scorpio DG, Akkoyunlu M, Fikrig E, Dumler JS. CXCR2 Blockade Influences Anaplasma phagocytophilum Propagation but Not Histopathology in the Mouse Model of Human Granulocytic Anaplasmosis. MSphere 2004, 11: 963-968. PMID: 15358660, PMCID: PMC515272, DOI: 10.1128/cdli.11.5.963-968.2004.Peer-Reviewed Original ResearchConceptsHuman granulocytic anaplasmosisControl miceGranulocytic anaplasmosisC3H-scid miceInfected cellsTissue loadsObligate intracellular bacteriumNeutrophil recruitmentNeutrophil secretionAntibody blockadeChemokine inductionHepatic pathologyLiver histopathologyInterleukin-8Tissue injuryMouse modelControl animalsDay 14Intracellular bacteriumMiceInfectionAnaplasma phagocytophilumA. phagocytophilumHistopathologyNeutrophils
2001
Borrelia burgdorferi-Induced Inflammation Facilitates Spirochete Adaptation and Variable Major Protein-Like Sequence Locus Recombination
Anguita J, Thomas V, Samanta S, Persinski R, Hernanz C, Barthold S, Fikrig E. Borrelia burgdorferi-Induced Inflammation Facilitates Spirochete Adaptation and Variable Major Protein-Like Sequence Locus Recombination. The Journal Of Immunology 2001, 167: 3383-3390. PMID: 11544329, PMCID: PMC4309988, DOI: 10.4049/jimmunol.167.6.3383.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, PhysiologicalAnimalsAntibodies, BacterialAntigens, BacterialAntigens, SurfaceBacterial ProteinsBase SequenceBorrelia burgdorferiCD4-Positive T-LymphocytesDNA, BacterialGene Expression RegulationImmune SeraImmunocompetenceInflammationInterferon-gammaInterleukin-12LipoproteinsLyme DiseaseMiceMice, Inbred C3HMice, KnockoutMolecular Sequence DataReceptors, InterferonRecombination, GeneticSequence AlignmentSequence Homology, Nucleic AcidConceptsImmunocompetent miceDeficient miceB. burgdorferi N40IFN-gammaRMurine immune responseIFN-gamma-mediated responsesIFN-gamma-mediated signalsSpirochetal burdensSpirochete clearanceIL-12Immune responseIFN-gammaControl animalsDifferential immunoscreeningMice resultsMiceVariable major proteinsRT-PCRVivo adaptationB. burgdorferiClearanceBorrelia burgdorferi gene expressionB. burgdorferi survivalAdministrationVivoExploitation of Interleukin-8-Induced Neutrophil Chemotaxis by the Agent of Human Granulocytic Ehrlichiosis
Akkoyunlu M, Malawista S, Anguita J, Fikrig E. Exploitation of Interleukin-8-Induced Neutrophil Chemotaxis by the Agent of Human Granulocytic Ehrlichiosis. Infection And Immunity 2001, 69: 5577-5588. PMID: 11500432, PMCID: PMC98672, DOI: 10.1128/iai.69.9.5577-5588.2001.Peer-Reviewed Original ResearchConceptsHuman granulocytic ehrlichiosisInterleukin-8Granulocytic ehrlichiosisHGE bacteriaUpregulation of CXCR2IL-8 receptorsIL-8 productionIL-8 secretionSite of infectionInfected HL-60 cellsObligate intracellular bacteriumChemotaxis chamber assayNeutrophils migrateNeutrophil migrationNeutrophil chemotaxisImmunodeficient miceControl animalsBacterial disseminationHost defensePromyelocytic cell lineChamber assayIntracellular bacteriumHL-60 cellsRetinoic acidNeutrophil lineage
1999
Selective Anti-Inflammatory Action of Interleukin-11 in Murine Lyme Disease: Arthritis Decreases while Carditis Persists
Anguita J, Barthold S, Samanta S, Ryan J, Fikrig E. Selective Anti-Inflammatory Action of Interleukin-11 in Murine Lyme Disease: Arthritis Decreases while Carditis Persists. The Journal Of Infectious Diseases 1999, 179: 734-737. PMID: 9952389, DOI: 10.1086/314613.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalAnti-Inflammatory AgentsArthritis, InfectiousFemaleHumansInflammationInterferon-gammaInterleukin-11Interleukin-12Interleukin-4Lyme DiseaseMiceMice, Inbred C3HMyocarditisNitric Oxide SynthaseNitric Oxide Synthase Type IIRecombinant ProteinsRNA, MessengerTranscription, GeneticConceptsMurine Lyme diseaseIL-11Potent anti-inflammatory propertiesInducible nitric oxide synthaseLyme diseaseMurine Lyme carditisAnti-inflammatory actionRole of interleukinAnti-inflammatory propertiesNitric oxide synthaseInnate immune responseB. burgdorferi-infected miceBurgdorferi-infected miceLyme carditisCardiac inflammationLyme arthritisIL-12Less arthritisIL-4Oxide synthaseBlocking antibodiesImmune responseControl animalsInterleukin-11Borrelia burgdorferi