2012
Spirochete antigens persist near cartilage after murine Lyme borreliosis therapy
Bockenstedt LK, Gonzalez DG, Haberman AM, Belperron AA. Spirochete antigens persist near cartilage after murine Lyme borreliosis therapy. Journal Of Clinical Investigation 2012, 122: 2652-2660. PMID: 22728937, PMCID: PMC3386809, DOI: 10.1172/jci58813.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnti-Bacterial AgentsAntigens, BacterialArthritis, InfectiousBacterial LoadBorrelia burgdorferiCartilageCeftriaxoneDoxycyclineEar, ExternalFemaleFluorescence Recovery After PhotobleachingGreen Fluorescent ProteinsJoint CapsuleLyme DiseaseMiceMice, Inbred C3HMice, Inbred C57BLMice, KnockoutMicroscopy, Fluorescence, MultiphotonMyeloid Differentiation Factor 88PatellaRecombinant ProteinsConceptsNaive miceAntibiotic treatmentIntravital microscopyAntibiotic-refractory Lyme arthritisLyme diseaseTNF-α productionBorrelia burgdorferi antigensB. burgdorferi antigensSpirochete antigenTLR responsivenessInflammatory arthritisAntibiotic therapyLyme arthritisWT miceMusculoskeletal symptomsAntigens persistSlow resolutionImmunodeficient miceMouse modelTissue transplantsPathogen burdenSpirochete DNAInfectious spirochetesLyme borreliosisMice
2009
The Caspase 1 Inflammasome Is Not Required for Control of Murine Lyme Borreliosis
Liu N, Belperron AA, Booth CJ, Bockenstedt LK. The Caspase 1 Inflammasome Is Not Required for Control of Murine Lyme Borreliosis. Infection And Immunity 2009, 77: 3320-3327. PMID: 19487481, PMCID: PMC2715671, DOI: 10.1128/iai.00100-09.Peer-Reviewed Original ResearchConceptsCaspase-1 inflammasomeCaspase-1Immune responseHost defenseLyme borreliosisToll-like receptor-mediated responsesDay 14 postinfectionPrevalence of arthritisT cell responsesApoptosis-associated speck-like proteinMild transient elevationBorrelia burgdorferiMurine Lyme borreliosisReceptor-mediated responsesCaspase-1 deficiencyC-terminal caspase recruitment domainSpeck-like proteinAbility of macrophagesEnzyme caspase-1IL-18Humoral immunityInterleukin-1betaTransient elevationPathogen burdenInflammasome
2007
Marginal Zone B-Cell Depletion Impairs Murine Host Defense against Borrelia burgdorferi Infection
Belperron AA, Dailey CM, Booth CJ, Bockenstedt LK. Marginal Zone B-Cell Depletion Impairs Murine Host Defense against Borrelia burgdorferi Infection. Infection And Immunity 2007, 75: 3354-3360. PMID: 17470546, PMCID: PMC1932939, DOI: 10.1128/iai.00422-07.Peer-Reviewed Original ResearchConceptsT-cell-independent antibodiesCell-depleted miceSplenic CD4Cell depletionPathogen burdenSplenic T cell responsesHost defenseT-cell activation markersC3H/HeJ miceImmunoglobulin M titersInfected control miceMurine host defensePathogen-specific IgMT cell responsesMarginal zone B cellsBlood-borne antigensBlood-borne pathogensWeeks of infectionB cell subsetsImmune mouse serumBorrelia burgdorferi infectionImportant host defenseSevere arthritisActivation markersControl mice
2005
Infection-Induced Marginal Zone B Cell Production of Borrelia hermsii-Specific Antibody Is Impaired in the Absence of CD1d
Belperron AA, Dailey CM, Bockenstedt LK. Infection-Induced Marginal Zone B Cell Production of Borrelia hermsii-Specific Antibody Is Impaired in the Absence of CD1d. The Journal Of Immunology 2005, 174: 5681-5686. PMID: 15843569, DOI: 10.4049/jimmunol.174.9.5681.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, BacterialAntibody SpecificityAntigens, CD1Antigens, CD1dB-Lymphocyte SubsetsBorreliaBorrelia InfectionsDNA, BacterialGerminal CenterImmune SeraImmunity, InnateImmunization, PassiveImmunoglobulin MLymphocyte ActivationLymphocyte DepletionMiceMice, Inbred C57BLMice, KnockoutConceptsMZB cellsActivation markersPathogen burdenMouse serumAbsence of CD1dBlood-borne AgsCD1d-deficient micePathogen-specific IgMActivation marker expressionMarginal zone B cellsT cell helpImmune mouse serumWild-type miceCritical host defenseB cell productionB. hermsiiCD1d expressionSerum levelsCell helpPassive transferSpirochete burdenAb productionSpirochete Borrelia burgdorferiB cellsCell activation
2004
Myeloid Differentiation Antigen 88 Deficiency Impairs Pathogen Clearance but Does Not Alter Inflammation in Borrelia burgdorferi-Infected Mice
Liu N, Montgomery RR, Barthold SW, Bockenstedt LK. Myeloid Differentiation Antigen 88 Deficiency Impairs Pathogen Clearance but Does Not Alter Inflammation in Borrelia burgdorferi-Infected Mice. Infection And Immunity 2004, 72: 3195-3203. PMID: 15155621, PMCID: PMC415708, DOI: 10.1128/iai.72.6.3195-3203.2004.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsAntibodies, BacterialAntigens, DifferentiationArthritisBorrelia burgdorferiDNA, BacterialInflammationLyme DiseaseMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88MyocarditisOpsonin ProteinsPhagocytosisReceptors, ImmunologicUrineConceptsToll-like receptor 2Days of infectionPathogen burdenWT miceAcute inflammationB. burgdorferi-specific antibodyPathogen-specific adaptive immunityMyD88-dependent signaling pathwaysTumor necrosis factor alphaBurgdorferi-specific antibodiesImmunoglobulin G1 responsesTLR2-deficient miceInnate immune cellsBorrelia burgdorferiNecrosis factor alphaWild-type miceIgM titersImmune cellsInflammatory responseFactor alphaAdaptive immunitySpirochete Borrelia burgdorferiWT macrophagesReceptor 2Pathogen clearance