2009
The Urokinase Receptor (uPAR) Facilitates Clearance of Borrelia burgdorferi
Hovius JW, Bijlsma MF, van der Windt GJ, Wiersinga WJ, Boukens BJ, Coumou J, Oei A, de Beer R, de Vos AF, van 't Veer C, van Dam AP, Wang P, Fikrig E, Levi MM, Roelofs JJ, van der Poll T. The Urokinase Receptor (uPAR) Facilitates Clearance of Borrelia burgdorferi. PLOS Pathogens 2009, 5: e1000447. PMID: 19461880, PMCID: PMC2678258, DOI: 10.1371/journal.ppat.1000447.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArthritis, InfectiousBorrelia burgdorferiCell MovementHeartHistocytochemistryHumansLeukocytesLyme DiseaseMiceMice, Inbred C57BLMice, KnockoutMyocarditisPhagocytosisReceptors, Urokinase Plasminogen ActivatorSkinStatistics, NonparametricUp-RegulationUrinary BladderUrokinase-Type Plasminogen ActivatorConceptsB. burgdorferi numbersWT controlsPhagocytotic capacityC3H/HeN backgroundIL-1beta mRNA expressionBorrelia burgdorferiB. burgdorferi infectionRole of uPARSevere carditisBurgdorferi infectionImmune responseLeukocyte functionSpirochete Borrelia burgdorferiFibrinolytic systemPAI-1Facilitate clearanceMRNA expressionHuman leukocytesLyme borreliosisMiceB. burgdorferiCausative agentProteinase receptorUPARAdequate eradication
2000
Borrelia burgdorferi Gene Expression In Vivo and Spirochete Pathogenicity
Anguita J, Samanta S, Revilla B, Suk K, Das S, Barthold S, Fikrig E. Borrelia burgdorferi Gene Expression In Vivo and Spirochete Pathogenicity. Infection And Immunity 2000, 68: 1222-1230. PMID: 10678930, PMCID: PMC97271, DOI: 10.1128/iai.68.3.1222-1230.2000.Peer-Reviewed Original ResearchConceptsC3H/HeN miceBorrelia burgdorferi spirochetesLyme disease pathogenesisNonpathogenic spirochetesSpirochete disseminationHumoral responseImmunocompetent miceHeN miceSCID miceC3H miceImmunodeficient miceImmune serumDisease pathogenesisCarditisArthritisMiceGene expressionGenomic expression libraryDiseaseB. burgdorferiB. burgdorferi N40Borrelia burgdorferi gene expressionMammalian infectionSubsequent developmentInfection
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 KeywordsAnimalsAnti-Inflammatory AgentsAntibodies, MonoclonalArthritis, 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
1998
Borrelia burgdorferi-Infected, Interleukin-6-Deficient Mice Have Decreased Th2 Responses and Increased Lyme Arthritis
Anguita J, Rincón M, Samanta S, Barthold S, Flavell R, Fikrig E. Borrelia burgdorferi-Infected, Interleukin-6-Deficient Mice Have Decreased Th2 Responses and Increased Lyme Arthritis. The Journal Of Infectious Diseases 1998, 178: 1512-1515. PMID: 9780277, DOI: 10.1086/314448.Peer-Reviewed Original ResearchConceptsIL-6-deficient miceLyme arthritisT cellsCell responsesCD4 T cell responsesT helper cell responsesInterleukin-6-deficient miceHelper cell responsesLess IL-4CD4 T cellsEffector Th2 cellsT cell responsesBorrelia burgdorferiNaive T cellsMurine Lyme arthritisDays of infectionJoint inflammationTh2 responsesArthritis incidenceIgG2b levelsC57BL/6 miceIL-6Th2 phenotypeIL-4Th2 cells