Central and peripheral nervous system infection, immunity, and inflammation in the NHP model of Lyme borreliosis.

 Ann Neurol. 2001 Sep;50,3, :330-8.Central and peripheral nervous system infection, 
immunity, and inflammation in the NHP model of Lyme borreliosis. Pachner AR, Cadavid D, 
Shu G, Dail D, Pachner S, Hodzic E, Barthold SW. Department of Neurosciences, UMDNJ-New 
Jersey Medical School, Newark 07103, USA. pachner@umdnj.edu
The relationship between chronic infection, antispirochetal immunity, and inflammation is 
unknown in Lyme neuroborreliosis. In the nonhuman primate model of Lyme neuroborreliosis, 
we measured spirochetal density in the nervous system and othe r tissues by polymerase chain 
reaction and correlated these values to anti-Borrelia burgdorferi antibody in the serum and 
cerebrospinal fluid, and to inflammation in tissues. Despite substantial presence of Borrelia
burgdorferi, the causative agent of Lyme borreliosis, in the central nervous system, only minor 
inflammation was present there, though skeletal and cardiac muscle, which contained similar 
levels of spirochete, were highly inflamed. Anti-Borrelia burgdoferi antibody was present in the 
cerebrospinal fluid but was not selectively concentrated. All infected animals developed 
anti-Borrelia burgdorferi antibody in the serum, but increased amplitude of antibody was not 
predictive of higher levels of infection. These data demonstrate that Lyme neuroborreliosis is a 
persistent infection, that spirochetal presence is a necessary but not sufficient condition for 
inflammation, and that antibody measured in serum may not predict the severity of infection




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