Group B streptococcal pilus proteins contribute to adherence to and invasion of brain microvascular endothelial cells

Surface filamentous structures known as pili have been discovered recently in the gram-positive strepto-coccal pathogens that cause invasive disease in humans, including group B Streptococcus (GBS). We show that two GBS proteins involved in pilus formation, encoded by pilA and pilB, also facilitate the interaction of this important agent of central nervous system infection with endothelial cells of the human blood-brain barrier. Group B Streptococcus (GBS), a gram-positive bacterial pathogen, is a major cause of meningitis in newborns. In order to cause central nervous system infection, blood-borne GBS must interact with and breech the blood-brain barrier (BBB), comprised primarily of a single layer of brain microvascular endothelial cells. While GBS adheres to and invades human brain microvascular endothelial cells (hBMEC) (9), the spe-cific GBS factors that contribute to this process are only be-ginning to be elucidated. Proper anchoring of lipoteichoic acid on the GBS surface facilitates hBMEC invasion, while the pore-forming -hemolysin/cytolysin is cytolytic for hBMEC