Type IV pili mediate the initial interaction of many bacterial pathogens with their host cells. In Neisseria meningitidis, the causative agent of cerebrospinal meningitis, type IV pili–mediated adhesion to brain endothelial cells is required for bacteria to cross the blood-brain barrier. Here, type IV pili–mediated adhesion of N. meningitidis to human brain endothelial cells was found to recruit the Par3/Par6/PKCζ polarity complex that plays a pivotal role in the establishment of eukaryotic cell polarity and the formation of intercellular junctions. This recruitment leads to the formation of ectopic intercellular junctional domains at the site of bacteria–host cell interaction and a subsequent depletion of junctional proteins at the cell-cell interface with opening of the intercellular junctions of the brain-endothelial interface.