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. Author manuscript; available in PMC: 2020 Mar 19.
Published in final edited form as: Semin Cell Dev Biol. 2016 Jul 19;60:155–167. doi: 10.1016/j.semcdb.2016.07.019

Fig. 1.

Fig. 1

Listeria intracellular cycle. Listeria surface invasion proteins interact with host cell receptors in epithelial cells triggering bacterial engulfment (A). Listeria transiently resides in an internalization vacuole (B), but bacterial secreted toxins lyse the vacuole (C) and bacteria are released in the host cell cytoplasm. Cytoplasmic bacteria multiply and polymerize host cell actin, promoting an actin-based motility system (D) which propels the bacteria and allows escape from the autophagic pathway (E). Upon reaching the host cell plasma membrane, Listeria induces the formation of protrusions (F) and are found in double-membrane vacuoles in secondary cells (G). Disruption of this compartment by bacterial secreted toxins allows the start of new infection cycle.