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Semin Neurol 1997; 17(1): 57-62
DOI: 10.1055/s-2008-1040914
© 1997 by Thieme Medical Publishers, Inc.

Mechanisms of Injury in Lyme Neuroborreliosis

Juan Carlos Garcia-Monco, Jorge L. Benach
  • Department of Neurology (J.C.G.-M.), Hospital de Galdacano, Vizcaya, Spain, and Department of Pathology, SUNY at Stony Brook, Stony Brook, New York
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Publication History

Publication Date:
19 March 2008 (online)

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ABSTRACT

Neurologic injury in infection with Borrelia burgdorferi can be due to the direct action of the spirochetes and spirochetal products on neural cells. There is in vitro evidence for the adherence of this organism to neurons, to glia, and to Schwann cells. Adhesion was found to be associated with galactocerebroside, a glycolipid component of myelin, and could act as a receptor for B. burgdorferi in oligodendroglia and in Schwann cells. Another pathway for neurologic injury could be through amplification of the inflammatory response by newly invading organisms (acute) and persisting (chronic) organisms. There is experimental evidence for production of IL-6, TNF-α, and nitric oxide by neural cells exposed to B. burgdorferi. Similar findings have been obtained from neuroborreliosis patients. Although less likely, there is the possibility that autoreactive mechanisms could have a role in the development of some manifestations of neuroborreliosis.

Keywords

Adhesion - inflammation - glia - nitric oxide - cytokines

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