Cytoskeletal mechanics during Shigella invasion and dissemination in epithelial cells.

The actin cytoskeleton is key to the barrier function of epithelial cells, by permitting the establishment and maintenance of cell-cell junctions and cell adhesion to the basal matrix. Actin exists under monomeric and polymerized filamentous form and its polymerization following activation of nucleation promoting factors generates pushing forces, required to propel intracellular microorganisms in the host cell cytosol or for the formation of cell extensions that engulf bacteria. Actin filaments can associate with adhesion receptors at the plasma membrane via cytoskeletal linkers. Membrane anchored to actin filaments are then subjected to the retrograde flow that may pull membrane-bound bacteria inside the cell. To induce its internalization by normally non-phagocytic cells, bacteria need to establish adhesive contacts and trick the cell into apply pulling forces, and/or to generate protrusive forces that deform the membrane surrounding its contact site. In this review, we will focus on recent findings on actin cytoskeleton reorganization within epithelial cells during invasion and cell-to-cell spreading by the enteroinvasive pathogen Shigella, the causative agent of bacillary dysentery.