April 16, 2015 American Journal of Pathology About 15 percent of patients with Lyme disease develop peripheral and central nervous system involvement, often accompanied by debilitating and painful symptoms. New research indicates that inflammation plays a causal role in the array of neurologic changes associated with Lyme disease. The investigators also showed that the anti-inflammatory drug dexamethasone prevents many of these reactions. http://www.sciencedaily.com/releases/2015/04/150416084338.htm The researchers examined the role of inflammation in the nervous systems of Bb-infected animals. Significantly elevated levels of the inflammatory mediators interleukin-6 (IL-6), IL-8, CCL2, and CXCL13 were observed, as well as pleocytosis (increased cell counts, primarily white blood cells) in the cerebrospinal fluid of all infected animals -- except in those treated with dexamethasone. "Chemokines such as IL-8 and CCL2 are known to mediate the influx of immune cells in the central nervous system compartment during bacterial meningitis, and CXCL13 is the major determinant of B cell recruitment into the cerebrospinal fluid during neuroinflammation," explained Dr. Philipp. Although antibiotics are the standard and necessary first-line treatment for Lyme disease, the results show the potential therapeutic impact of anti-inflammatory or immune-modulatory agents for Lyme-related neuroborreliosis. Most of the neuropathological changes produced by Bb infection were prevented by dexamethasone, a broad-spectrum steroidal anti-inflammatory drug "Our results suggest that ongoing cytokine activation in the nervous system can contribute to the persistent symptoms of fatigue, pain, and cognitive dysfunction that patients sometimes experience despite having been treated for Lyme disease."