2011
O4-S2.05 Myd-88 deficient mice show evidence of productive T pallidum infection"
Dunne D, Silver A, Fieber J, Zeiss C, Fikrig E. O4-S2.05 Myd-88 deficient mice show evidence of productive T pallidum infection". Sexually Transmitted Infections 2011, 87: a87. DOI: 10.1136/sextrans-2011-050109.149.Peer-Reviewed Original ResearchMyD-88C57BL/6 miceDeficient miceImmunohistochemical stainsImmune responseMurine modelT pallidumDay 10Intact innate immune responseOnly natural reservoirNew Zealand male rabbitsB6 control miceInnate immune cellsUseful murine modelAged C57BL/6 miceWild-type miceInnate immune responseInnate immune systemPattern recognition receptorsImmune response mechanismsDownstream cytokine responsesSyphilis infectionSystemic illnessLymph nodesCytokine responses
2008
Borrelia burgdorferi lipoprotein BmpA activates pro-inflammatory responses in human synovial cells through a protein moiety
Yang X, Izadi H, Coleman AS, Wang P, Ma Y, Fikrig E, Anguita J, Pal U. Borrelia burgdorferi lipoprotein BmpA activates pro-inflammatory responses in human synovial cells through a protein moiety. Microbes And Infection 2008, 10: 1300-1308. PMID: 18725314, PMCID: PMC2648844, DOI: 10.1016/j.micinf.2008.07.029.Peer-Reviewed Original ResearchConceptsB mutantsWild-type B. burgdorferiP38 MAP kinase pathwayMAP kinase pathwayHuman synovial cellsSynovial cellsProtein moietyP38 MAP kinaseNF-kappaBLyme arthritisB operonKinase pathwayMAP kinaseRecombinant BmpAPro-inflammatory cytokines TNF-alphaCultured human synovial cellsLipopolysaccharide inhibitorMutantsCytokines TNF-alphaHost inflammatory responsePro-inflammatory responseCytokine responsesIL-1betaTNF-alphaInflammatory response
2002
Cyclooxygenase 2 activity modulates the severity of murine Lyme arthritis
Anguita J, Samanta S, Ananthanarayanan SK, Revilla B, Geba GP, Barthold SW, Fikrig E. Cyclooxygenase 2 activity modulates the severity of murine Lyme arthritis. Pathogens And Disease 2002, 34: 187-191. PMID: 12423770, PMCID: PMC4307933, DOI: 10.1111/j.1574-695x.2002.tb00623.x.Peer-Reviewed Original ResearchConceptsJoint inflammationCOX-2B. burgdorferi-specific antibodyBurgdorferi-specific antibodiesOnset of arthritisDegree of inflammationNoninfectious inflammatory diseasesCyclooxygenase-2 activityCOX-2 activityB. burgdorferiCOX-2 gene expressionMurine Lyme arthritisSpecific inhibitionLyme arthritisCytokine responsesInfectious arthritisRheumatoid arthritisInfected miceInflammatory diseasesInducible isoformMurine jointsArthritisInflammationMRNA expressionLyme disease
2000
Gamma Interferon Dominates the Murine Cytokine Response to the Agent of Human Granulocytic Ehrlichiosis and Helps To Control the Degree of Early Rickettsemia
Akkoyunlu M, Fikrig E. Gamma Interferon Dominates the Murine Cytokine Response to the Agent of Human Granulocytic Ehrlichiosis and Helps To Control the Degree of Early Rickettsemia. Infection And Immunity 2000, 68: 1827-1833. PMID: 10722570, PMCID: PMC97354, DOI: 10.1128/iai.68.4.1827-1833.2000.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBacteremiaConcanavalin ACytokinesDisease ProgressionDose-Response Relationship, DrugEhrlichiosisEnzyme-Linked Immunosorbent AssayFemaleHL-60 CellsHumansImmunoglobulin GInterferon-gammaMiceMice, Inbred C3HNeutrophilsReverse Transcriptase Polymerase Chain ReactionRickettsiaSpleenTime FactorsT-LymphocytesConceptsIFN-gamma-deficient miceHuman granulocytic ehrlichiosisIFN-gamma levelsDay 8Cytokine responsesIFN-gammaGamma interferonCells/HGE bacteriaGranulocytic ehrlichiosisIFN-gamma-independent mechanismMurine cytokine responsesTime pointsAgent of HGEMore IFN-gammaC3H/HeNLess interleukin-4IFN-gamma responsesMurine infection modelLater time pointsObligate intracellular bacteriumTh1 phenotypeC57BL/6 miceDNA burdenImmunocompetent mice