To examine the amount of cellular autophagy induced by L. monocytogenes, we monitored the conversion of LC3-I to LC3-II in wild-type bone marrow derived macrophages (BMDMs) isolated from C57/B6 mice, infected with L. monocytogenes [25, 26] . Activation of autophagy triggers LC3-I lipidation resulting in the conversion of LC3-I to LC3-II, which is measured by a mobility shift on SDS-PAGE [27] . Within 40 minutes of infection with wild-type L. monocytogenes, the amount of LC3-II increased compared to uninfected cells (Fig. 1A) . Dhly (LLO-minus) L. monocytogenes and heat-killed bacteria stimulated almost no LC3-I to LC3-II conversion, as compared to wild-type L. monocytogenes over a 60 minute time course of infection ( Fig. 1B and data not shown) . Therefore, we concluded that while infection alone induced very little autophagy, wild-type bacteria secreting LLO induced increased amounts of autophagy. Further, we found that during a 60-minute infection, the absence of the bacterial proteins ActA and either of the phospholipases did not significantly affect the amount of autophagy activation as measured by LC3-I lipidation (Fig. 1B) .