ArticleJournal of neuroinflammation2009
Possible role of glial cells in the onset and progression of Lyme neuroborreliosis.
Article in Journal of neuroinflammation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
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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.
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Who cites it
52 citing papers in PubMed, 85 citations in OpenAlex.
- Innate Immune Evasion of Lyme Disease Pathogen Drives Alzheimer-Like Pathology.Research square · 2026Article
- Article
- Audio-Vestibular Function in Patients Diagnosed with Lyme Neuroborreliosis.The journal of international advanced otology · 2025Article
- CXCL13/CXCR5: a new target for pain treatment.International journal of surgery (London, England) · 2025Review
- Cerebrospinal fluid protein profiling of inflammatory and neurobiological markers in Lyme neuroborreliosis.Scientific reports · 2025Article
- High efficacy therapy to prevent the formation of meningeal tertiary lymphoid organs after CXCL13 index screening in early multiple sclerosis.Frontiers in neuroscience · 2025Article
- Cerebrospinal Fluid Cytology in Lyme Neuroborreliosis Revisited-Role of Neutrophilic Granulocytes: A Retrospective Single-Center Study.Journal of clinical medicine · 2024Article
- Bridging the gap: Insights in the immunopathology of Lyme borreliosis.European journal of immunology · 2024Review
- Dysautonomia following Lyme disease: a key component of post-treatment Lyme disease syndrome?Frontiers in neurology · 2024Review
- Fibroblast growth factor receptor inhibitors mitigate the neuropathogenicity ofFrontiers in immunology · 2024Article
- Inflammation and immunomodulation in central nervous system injury - B cells as a novel therapeutic opportunity.Neurobiology of disease · 2023Review
- Lyme disease and the pursuit of a clinical cure.Frontiers in medicine · 2023Review
- Comparative proteomics profiling revealed the involvement of GRB2-ROCK2 axis in Lyme neuroborreliosis caused by Borrelia Burgdorferi.Journal of cellular and molecular medicine · 2022Article
- Borrelia burgdorferi Co-Localizing with Amyloid Markers in Alzheimer's Disease Brain Tissues.Journal of Alzheimer's disease : JAD · 2022Article
- CXCR5 down-regulation alleviates cognitive dysfunction in a mouse model of sepsis-associated encephalopathy: potential role of microglial autophagy and the p38MAPK/NF-κB/STAT3 signaling pathway.Journal of neuroinflammation · 2021Article
- Lyme Neuroborreliosis: Mechanisms ofBrain sciences · 2021Review
- CXCL13/CXCR5 signalling is pivotal to preserve motor neurons in amyotrophic lateral sclerosis.EBioMedicine · 2020Article
- Resveratrol and Neuroprotection: Impact and Its Therapeutic Potential in Alzheimer's Disease.Frontiers in pharmacology · 2020Review
- Symptom Clusters and Functional Impairment in Individuals Treated for Lyme Borreliosis.Frontiers in medicine · 2020Article
- Protozoan ParasiteFrontiers in microbiology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundLyme neuroborreliosis (LNB) may present as meningitis, cranial neuropathy, acute radiculoneuropathy or, rarely, as encephalomyelitis. We hypothesized that glia, upon exposure to Borrelia burgdorferi, the Lyme disease agent, produce inflammatory mediators that promote the acute cellular infiltration of early LNB. This inflammatory context could potentiate glial and neuronal apoptosis.
methodsWe inoculated live B. burgdorferi into the cisterna magna of rhesus macaques and examined the inflammatory changes induced in the central nervous system (CNS), and dorsal root nerves and ganglia (DRG).
resultsELISA of the cerebrospinal fluid (CSF) showed elevated IL-6, IL-8, CCL2, and CXCL13 as early as one week post-inoculation, accompanied by primarily lymphocytic and monocytic pleocytosis. In contrast, onset of the acquired immune response, evidenced by anti-B. burgdorferi C6 serum antibodies, was first detectable after 3 weeks post-inoculation. CSF cell pellets and CNS tissues were culture-positive for B. burgdorferi. Histopathology revealed signs of acute LNB: severe multifocal leptomeningitis, radiculitis, and DRG inflammatory lesions. Immunofluorescence staining and confocal microscopy detected B. burgdorferi antigen in the CNS and DRG. IL-6 was observed in astrocytes and neurons in the spinal cord, and in neurons in the DRG of infected animals. CCL2 and CXCL13 were found in microglia as well as in endothelial cells, macrophages and T cells. Importantly, the DRG of infected animals showed significant satellite cell and neuronal apoptosis.
conclusionOur results support the notion that innate responses of glia to B. burgdorferi initiate/mediate the inflammation seen in acute LNB, and show that neuronal apoptosis occurs in this context.
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What OpenQuestion holds
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.