The relatively few number of organisms in the CNS has further limited our ability to directly examine spirochete gene expression in the nervous system.To overcome this limitation, we have exploited differential expression analysis by using a custom-amplified library (DECAL) (36, 39).DECAL, a technique to selectively amplify specific prokaryotic transcriptomes, was first used for the global analysis of gene expression in (39).
Neurological symptoms are common manifestations of Lyme disease; however, the paucibacillary nature of the spirochete in this environment has precluded a molecular analysis of the spirochete in the CNS.
We have now adapted differential expression analysis by using a custom-amplified library (DECAL) in conjunction with was examined in the CNS and heart of steroid-treated and immunocompetent NHPs.
Eighty-six chromosomal genes and 80 plasmid-encoded genes were expressed at similar levels in the CNS and heart tissue of both immunocompetent and steroid-treated NHPs.
The expression of 66 chromosomal genes and 32 plasmid-encoded genes was increased in the CNS of both immunocompetent and steroid-treated NHPs.
It is likely that the expression of these genes is governed by physiological factors specific to the CNS milieu.
However, 83 chromosomal and 114 plasmid-encoded genes showed contrasting expression profiles in steroid-treated and immunocompetent NHPs.
The effect of dexamethasone on the immune status of the host as well as on the host metabolic pathways could contribute to these differences in the (1), can involve the skin, joints, heart, and nervous system (2).
The manifestations of neuroborreliosis include facial palsy, aseptic meningitis, cranial neuritis, peripheral neuropathy, radiculopathy, and encephalitis (3, 4).
The pathogenesis of neuroborreliosis is multifactorial and likely related to the persistence of a small number of spirochetes in the CNS and the host response to (5).
Despite intensive clinical and basic research on neuroborreliosis, questions concerning its diagnosis, treatment, and pathogenesis remain unanswered.
The understanding of Lyme disease has been aided by several animal models, most notably the murine model (6–8).