Shigella, the causative agent of bacillary dysentery, invades epithelial ce
lls by reorganizing the cell cytoskeleton during bacterial entry. This entr
y process requires the Shigella Ipa proteins that are secreted by a type II
I secretion apparatus and that act in concert to fine tune cell responses.
Actin polymerization at the site oi entry is dependent on the IpaB and IpaC
proteins, whereas IpaA further modulates cytoskeletal rearrangements by bi
nding to vinculin.