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Fig. 8. Schematic representation of the signalling pathways activated by N. meningitidis and involved in bacterial entry into endothelial cells. Type-IV pili initiate the interaction of virulent, encapsulated N. meningitidis with human endothelial cells by interacting with a cellular receptor, possibly CD46 (Kallstrom et al., 1997). This pilus-dependent adhesion induces the recruitment of ezrin and the clustering of several transmembrane proteins: the ErbB2 tyrosine-kinase receptor and the ezrin-binding proteins CD44 and ICAM-1. The activation of both Rho and Cdc42 GTPases induces a local polymerization of cortical actin. ErbB2 clustering leads to the activation of Src tyrosine kinase. In parallel, LOS of N. meningitidis, by a mechanism which remains to be identified, provides a co-stimulatory signal leading to PI3K and Rac1 activation, and the subsequent translocation of cortactin to site of cortical actin rearrangements. When localized to the cell plasma membrane, cortactin is tyrosine phosphorylated by Src kinase and contributes to the formation of dynamic actin structures, leading to the formation of membrane projections that surround bacteria and provoke their internalization within endothelial intracellular vacuoles

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