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Possible role of glial cells in the onset and progression of Lyme neuroborreliosis.
J Neuroinflammation. 2009 Aug 25; 6:23.JN

Abstract

BACKGROUND

Lyme 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.

METHODS

We 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).

RESULTS

ELISA 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.

CONCLUSION

Our 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.

Authors+Show Affiliations

Division of Bacteriology and Parasitology, Tulane National Primate Research Center, Covington, LA, USA. gramesh@tulane.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

19706181

Citation

Ramesh, Geeta, et al. "Possible Role of Glial Cells in the Onset and Progression of Lyme Neuroborreliosis." Journal of Neuroinflammation, vol. 6, 2009, p. 23.
Ramesh G, Borda JT, Gill A, et al. Possible role of glial cells in the onset and progression of Lyme neuroborreliosis. J Neuroinflammation. 2009;6:23.
Ramesh, G., Borda, J. T., Gill, A., Ribka, E. P., Morici, L. A., Mottram, P., Martin, D. S., Jacobs, M. B., Didier, P. J., & Philipp, M. T. (2009). Possible role of glial cells in the onset and progression of Lyme neuroborreliosis. Journal of Neuroinflammation, 6, 23. https://doi.org/10.1186/1742-2094-6-23
Ramesh G, et al. Possible Role of Glial Cells in the Onset and Progression of Lyme Neuroborreliosis. J Neuroinflammation. 2009 Aug 25;6:23. PubMed PMID: 19706181.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Possible role of glial cells in the onset and progression of Lyme neuroborreliosis. AU - Ramesh,Geeta, AU - Borda,Juan T, AU - Gill,Amy, AU - Ribka,Erin P, AU - Morici,Lisa A, AU - Mottram,Peter, AU - Martin,Dale S, AU - Jacobs,Mary B, AU - Didier,Peter J, AU - Philipp,Mario T, Y1 - 2009/08/25/ PY - 2009/07/24/received PY - 2009/08/25/accepted PY - 2009/8/27/entrez PY - 2009/8/27/pubmed PY - 2009/11/17/medline SP - 23 EP - 23 JF - Journal of neuroinflammation JO - J Neuroinflammation VL - 6 N2 - BACKGROUND: Lyme 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. METHODS: We 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). RESULTS: ELISA 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. CONCLUSION: Our 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. SN - 1742-2094 UR - https://www.unboundmedicine.com/medline/citation/19706181/Possible_role_of_glial_cells_in_the_onset_and_progression_of_Lyme_neuroborreliosis_ L2 - https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-6-23 DB - PRIME DP - Unbound Medicine ER -