Interaction of Neisseria maningitidis with the components of the blood-brain barrier correlates with an increased expression of PilC.

A fatal untreated case of fulminant meningococcemia was examined to investigate the crossing of the blood-brain barrier (BBB) by Neisseria meningitidis. Microscopic examination showed bacteria in vivo adhering to the endothelium of both the choroid plexus and the meninges. Comparison of the isolates cultivated from the blood and the cerebrospinal fluid (CSF) revealed no antigenic variation of the pilin or the class 5 protein, whereas the expression of the PilC protein was greater in the CSF and the choroid plexus than in the blood. This was due to an increased activity of one of the pilC promotors. This higher expression of PilC correlated in vitro with greater adhesiveness to endothelial cells. A mutation in the single pilC locus of this strain abolished in vitro pilus-mediated adhesion to endothelial cells. These data suggest that PilC plays an important role in the crossing of the BBB, likely through pilus-mediated adhesion.