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 TransductionT-Lymphocytes, RegulatoryTh1 CellsConceptsA. 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
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
1994
Fc- And Non-Fc-Mediated Phagocytosis Of Borrelia Burgdorferi By Maerophages
Montgomery R, Nathanson M, Malawista S. Fc- And Non-Fc-Mediated Phagocytosis Of Borrelia Burgdorferi By Maerophages. The Journal Of Infectious Diseases 1994, 170: 890-893. PMID: 7930732, DOI: 10.1093/infdis/170.4.890.Peer-Reviewed Original ResearchConceptsConfocal fluorescence microscopyLyme disease spirocheteB. burgdorferiFluorescence microscopyBacterial surface antigensFc receptorsSurface antigenMacrophagesBorrelia burgdorferiSpirochetesBurgdorferiMajor roleSimilar lackComparable efficiencyUptakeColocalizationPhagocytosisInfectionAntigenLocalization
1993
The fate of Borrelia burgdorferi, the agent for Lyme disease, in mouse macrophages. Destruction, survival, recovery.
Montgomery RR, Nathanson MH, Malawista SE. The fate of Borrelia burgdorferi, the agent for Lyme disease, in mouse macrophages. Destruction, survival, recovery. The Journal Of Immunology 1993, 150: 909-15. PMID: 8423346, DOI: 10.4049/jimmunol.150.3.909.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBorrelia burgdorferi GroupCells, CulturedMacrophagesMiceMicroscopy, FluorescencePhagocytosisRabbitsConceptsUptake of spirochetesConfocal fluorescence microscopyLikely candidate siteEndocytic pathwayB. burgdorferiBorrelia burgdorferiFluorescence microscopyIntracellular persistenceLyme diseaseInfected cellsPersistence of spirochetesMouse macrophagesIntracellular organismsPositive compartmentsPossible pathogenetic mechanismsExtracellular organismsOrganismsAcridine orangeCellsMultiple time pointsPathogenetic mechanismsSpirochetesInfectious agentsCompartmentsLyme spirochete
1992
Evidence for reactive nitrogen intermediates in killing of staphylococci by human neutrophil cytoplasts. A new microbicidal pathway for polymorphonuclear leukocytes.
Malawista SE, Montgomery RR, van Blaricom G. Evidence for reactive nitrogen intermediates in killing of staphylococci by human neutrophil cytoplasts. A new microbicidal pathway for polymorphonuclear leukocytes. Journal Of Clinical Investigation 1992, 90: 631-636. PMID: 1379614, PMCID: PMC443143, DOI: 10.1172/jci115903.Peer-Reviewed Original ResearchConceptsReactive nitrogen intermediatesL-arginineNitric oxide synthase inhibitor NGranule-poor cytoplastsKilling of staphylococciNitrogen intermediatesSynthase inhibitor NEffect of NMMAChronic granulomatous diseaseHuman blood neutrophilsHuman neutrophil cytoplastsBlood neutrophilsGranulomatous diseasePolymorphonuclear leukocytesD-arginineIntact PMNsNeutrophil cytoplastsMicrobicidal pathwaysNMMASusceptible targetsMin of incubationModest decreaseInhibitor NStaphylococciOxidase activity
1989
Endocytic and Secretory Repertoire of the Lipid-Loaded Macrophage
Montgomery R, Cohn Z. Endocytic and Secretory Repertoire of the Lipid-Loaded Macrophage. Journal Of Leukocyte Biology 1989, 45: 129-138. PMID: 2492592, DOI: 10.1002/jlb.45.2.129.Peer-Reviewed Original ResearchConceptsLipid-laden cellsOil Red O stainingTumor necrosis factorArachidonic acid metabolitesRed O stainingIntracellular lipid poolsWestern blot analysisIntracellular lipid storageMouse peritoneal macrophagesCholesterol levelsNecrosis factorMacrophage functionO stainingScavenger receptorsSecretory functionAcid metabolitesAtherosclerotic arteriesPeritoneal macrophagesFunctional changesFibrinolytic activitySheep erythrocytesCholesterol acceptorsMacrophagesSecretory productsLipid storage