We hypothesized that a damaged phagosomal membrane was targeted by autophagy and that this interaction could ultimately affect the ability of the bacteria to survive inside of cells and/or escape from a phagosome. The capacity of L. monocytogenes to escape from phagocytic vacuoles was examined in both fibroblasts and macrophages that lacked functional autophagy due to the targeted disruption of the essential autophagy gene atg5 [33, 34] . L. monocytogenes escaped at an increased rate from primary vacuoles in the presence of autophagy in MEFs (Fig. 5A ). In contrast, the presence of autophagy had no measurable effect on escape rates in bone marrow-derived macrophages (Fig. 5B) . Further, contrary to a previous report, bacterial mutants lacking the secreted phospholipases that contribute to vacuolar escape had similar levels of cytosolic entry in both wild-type and atg5 2/2 MEFs as well as BMDMs (Fig. 5A, B) [24] . Finally, autophagy did not significantly affect the growth of wild-type L. monocytogenes in either MEFs or BMDMs (Fig. 5C, D) . Therefore, while LLO stimulated autophagy, there was no observable consequence in bacterial escape or growth in BMDMs. However, the decreased escape observed in atg5 2/2 MEFs suggests that under some conditions, autophagy may enhance, rather than prevent, bacterial escape.