2011
Age‐associated elevation in TLR5 leads to increased inflammatory responses in the elderly
Qian F, Wang X, Zhang L, Chen S, Piecychna M, Allore H, Bockenstedt L, Malawista S, Bucala R, Shaw AC, Fikrig E, Montgomery RR. Age‐associated elevation in TLR5 leads to increased inflammatory responses in the elderly. Aging Cell 2011, 11: 104-110. PMID: 22023165, PMCID: PMC3257374, DOI: 10.1111/j.1474-9726.2011.00759.x.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAgingExtracellular Signal-Regulated MAP KinasesFemaleHumansInflammationInterleukin-8MaleMiddle AgedMonocytesMultivariate AnalysisNF-kappa BP38 Mitogen-Activated Protein KinasesPhosphorylationProtein TransportRNA, MessengerSignal TransductionToll-Like Receptor 5Tumor Necrosis Factor-alphaConceptsToll-like receptorsIL-8Multivariable mixed-effects modelsOlder individualsElevated IL-8Levels of TLR5Expression of TLR5Production of TNFAge-associated elevationAge-related decreaseDendritic cellsImmune responsivenessElderly donorsInflammatory responseImmune functionNF-κBTLR5Progressive declineMonocytesMixed effects modelsMAPK p38Significant increaseEffects modelAssociated increaseCritical mechanism
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
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