ArticleThe American journal of pathology2008
Interaction of the Lyme disease spirochete Borrelia burgdorferi with brain parenchyma elicits inflammatory mediators from glial cells as well as glial and neuronal apoptosis.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 108 citations in OpenAlex.
- Modeling Immunity In Vitro: Slices, Chips, and Engineered Tissues.Annual review of biomedical engineering · 2021Pooled it
- Metabolites of prostaglandin synthases as potential biomarkers of Lyme disease severity and symptom resolution.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Pooled it
- Cerebrospinal fluid protein profiling of inflammatory and neurobiological markers in Lyme neuroborreliosis.Scientific reports · 2025Article
- Virulence of Burkholderia pseudomallei ATS2021 Unintentionally Imported to United States in Aromatherapy Spray.Emerging infectious diseases · 2024Article
- Direct Detection of Borrelia Species in Tissues.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Dysautonomia following Lyme disease: a key component of post-treatment Lyme disease syndrome?Frontiers in neurology · 2024Review
- Nisin a probiotic bacteriocin mitigates brain microbiome dysbiosis and Alzheimer's disease-like neuroinflammation triggered by periodontal disease.Journal of neuroinflammation · 2023Article
- Differential transcriptome response of blood brain barrier spheroids to neuroinvasiveFrontiers in cellular and infection microbiology · 2023Article
- Lyme disease and the pursuit of a clinical cure.Frontiers in medicine · 2023Review
- Implications of Microorganisms in Alzheimer's Disease.Current issues in molecular biology · 2022Review
- Does Dementia Have a Microbial Cause?NeuroSci · 2022Review
- Neuropathogenicity of non-viable Borrelia burgdorferi ex vivo.Scientific reports · 2022Article
- Lyme Neuroborreliosis: Mechanisms ofBrain sciences · 2021Review
- Host transcriptome response to Borrelia burgdorferi sensu lato.Ticks and tick-borne diseases · 2021Review
- Lyme Disease in Humans.Current issues in molecular biology · 2021Article
- Proteomic Analysis of Rhesus Macaque Brain Explants Treated WithFrontiers in cellular and infection microbiology · 2021Article
- Detecting Borrelia Spirochetes: A Case Study With Validation Among Autopsy Specimens.Frontiers in neurology · 2021Article
- Presentation of Acrodermatitis Chronica Atrophicans Rashes on Lyme Disease Patients in Canada.Healthcare (Basel, Switzerland) · 2020Article
- Effect ofAntibiotics (Basel, Switzerland) · 2020Article
- Monitoring of Nesting Songbirds Detects Established Population of Blacklegged Ticks and Associated Lyme Disease Endemic Area in Canada.Healthcare (Basel, Switzerland) · 2020Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Lyme neuroborreliosis, caused by the spirochete Borrelia burgdorferi, often manifests by causing neurocognitive deficits. As a possible mechanism for Lyme neuroborreliosis, we hypothesized that B. burgdorferi induces the production of inflammatory mediators in the central nervous system with concomitant neuronal and/or glial apoptosis. To test our hypothesis, we constructed an ex vivo model that consisted of freshly collected slices from brain cortex of a rhesus macaque and allowed live B. burgdorferi to penetrate the tissue. Numerous transcripts of genes that regulate inflammation as well as oligodendrocyte and neuronal apoptosis were significantly altered as assessed by DNA microarray analysis. Transcription level increases of 7.43-fold (P = 0.005) for the cytokine tumor necrosis factor-alpha and 2.31-fold (P = 0.016) for the chemokine interleukin (IL)-8 were also detected by real-time-polymerase chain reaction array analysis. The immune mediators IL-6, IL-8, IL-1beta, COX-2, and CXCL13 were visualized in glial cells in situ by immunofluorescence staining and confocal microscopy. Concomitantly, significant proportions of both oligodendrocytes and neurons undergoing apoptosis were present in spirochete-stimulated tissues. IL-6 production by astrocytes in addition to oligodendrocyte apoptosis were also detected, albeit at lower levels, in rhesus macaques that had received in vivo intraparenchymal stereotaxic inoculations of live B. burgdorferi. These results provide proof of concept for our hypothesis that B. burgdorferi produces inflammatory mediators in the central nervous system, accompanied by glial and neuronal apoptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.