Can the symptoms and signs of nervous system infection caused by Lyme disease be prevented in experimental animals by immune modulation?

Investigators studied this question in rhesus macaques by inoculating live Borrelia burgdorferi, the agent of Lyme disease, into the spinal canal and reported their results in the American Journal of Pathology this past year (Am J Pathol 2015, 185: 1344e1360; http://dx.doi.org/10.1016/j.ajpath.2015.01.024). Some animals were treated with the anti-inflammatory drug, dexamethasone, a corticosteroid that inhibits the expression of several immune mediators, and others were infected and untreated. Antibiotics were not given because the goal was to determine whether infection-induced damage in the nervous system was amenable to immune modulation alone. The animals were studied at 8- and 14-weeks post-inoculation. Enzyme-linked immunosorbent assay (ELISA) of cerebrospinal fluid showed significantly elevated levels of interleukin (IL)-6, IL-8, chemokine ligand 2, and CXCL 13 and pleocytosis in the infected animals that were untreated with immunotherapy but not in those given dexamethasone. Those without dexamethasone pretreatment developed leptomeningitis, vasculitis, and focal inflammation of the brain, spinal cord, and nerve roots indicative of neuronal and glial cell death. These changes were absent in the dexamethasone-pretreated animals. In accordance with their hypothesis, the investigators noted that experimental suppression of inflammation in the course of Lyme disease could be obtained by dexamethasone pretreatment to prevent infection-induced activation of the immune system.

Thus it is likely that vigorous host immunity in response to infection by Borrelia burgdorferi leads to the symptoms, signs, and pathological changed in the nervous system.