Fig. 9.1.

Depiction of the canonical intracellular lifecycle of L. monocytogenes. L. monocytogenes expresses virulence factors that orchestrate the various stages of its intracellular lifecycle [33, 34, 90, 188]. The surface proteins InlA and InlB facilitate L. monocytogenes internalization into normally nonphagocytic cells. Additional virulence factors, such as the secreted CDC toxin LLO, also mediate L. monocytogenes entry into host cells (cell 1) [33, 89]. Secreted in the primary vacuole, LLO, PI-PLC, and PC-PLC target and disrupt the vacuolar membrane to release the bacterium into the cytosol. In the cytosol, L. monocytogenes replicates, while avoiding autophagy recognition by recruiting the host proteins F-actin and the major vault protein, through interaction with the bacterial surface proteins ActA and InlK, respectively [116]. ActA recruits the host F-actin polymerization machinery at one pole of the bacterium. F-actin-mediated propulsion of the bacterium leads to the formation of an intercellular protrusion; this process is facilitated by the bacterial protein InlC that decreases the plasma membrane surface tension [189]. The resulting intercellular protrusion is ingested by the adjacent cell (cell 2). LLO and the phospholipases (PI-PLC and PC-PLC) disrupt the newly formed secondary vacuole to release the bacterium into the cytosol, where it repeats its intracellular lifecycle (Host proteins are italicized)