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Abstract
Neurological manifestations of Lyme disease (or neuroborreliosis) occur variably and
while it is clear that Borrelia burgdorferi can invade the nervous system, how it
does so is not well understood. Pathogen penetration through the blood brain barrier
(BBB) is often influenced by calcium signaling in the endothelial cells triggered
by extracellular host-pathogen interactions. We examined the traversal of B. burgdorferi
across the human BBB using in vitro model systems constructed of human brain microvascular
endothelial cells (HBMEC) grown on Costar Transwell inserts. Pretreatment of the cell
monolayers with BAPTA-AM (an intracellular calcium chelator) or phospholipase C (PLC)
inhibitor U73122 inhibited B. burgdorferi transmigration. By 5 h, BAPTA-AM significantly
inhibited (82-99%; p <0.017) spirochete traversal of HBMEC compared to DMSO controls.
Spirochete traversal was almost totally blocked (> or =99%; p <0.017) after pretreatment
with the PLC-beta inhibitor U73122 as a result of barrier tightening based on electric
cell-substrate impedance sensing (ECIS). The data suggest a role for calcium signaling
in CNS spirochete invasion through endothelial cell barriers.