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
