Mechanisms of Cellular Invasion
N. meningitidis is an intracellular human-specific pathogen responsible for septicemia and meningitis. Like most bacterial intracellular pathogens, N. meningitidis exploits host cell signaling pathways to promote its uptake by host cells. The signaling leading to bacterial internalization is induced by the type IV pili, which are the main means of meningococcal adhesion onto host cells. The signaling induced following Type IV pilus-mediated adhesion is responsible for the formation of microvilli-like structures at the site of the bacterial-cell interaction. These microvilli trigger the internalization of the bacteria into host cells. A major consequence of these signaling events is a reorganization of the actin cytoskeleton, which leads to the formation of membrane protrusions, engulfing bacterial pathogens into intracellular vacuoles. Efficient internalization of N. meningitidis also requires the activation of an alternative signaling pathway coupled with the activation of the tyrosine kinase receptor ErbB2. Beside Type IV pili, other outer membrane proteins may be involved in other mechanism of bacteria internalization into cells.
Read more about this topic: Neisseria Meningitidis
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