Neisserial porin (PorB) causes rapid calcium influx in target cells and induces apoptosis by the activation of cysteine proteases

The porin (PorB) of Neisseria gonorrhoeae is an intriguing bacterial factor owing to its ability to translocate from the outer bacterial membrane into host cell membranes where it modulates the infection process. Here we repo rt on the induction of programmed cell death after prolonged infection of e pithelial cells with pathogenic Neisseria species. The underlying mechanism we propose includes translocation of the porin, a transient increase in cy tosolic Ca2+ and subsequent activation of the Ca2+ dependent protease calpa in as well as proteases of the caspase family. Blocking the porin channel b y ATP eliminates the Ca2+ signal and also abolishes its pro-apoptotic funct ion. The neisserial porins share structural and functional homologies with the mitochondrial voltage-dependent anion channels (VDAC). The neisserial p orin may be an analogue or precursor of the ancient permeability transition pore, the putative central regulator of apoptosis.