There is mounting evidence that autophagy contributes to the innate immune response to microbial pathogens [16] [17] [18] . Pathogens that grow and or reside in the cytosol, such as: Shigella flexneri, Francisella tularensis, and Group A Streptococci lyse the host phagosomal membrane, escape into the cytosol and subsequently induce autophagy, as measured by LC3 colocalization, lipidation and electron microscopy [35] [36] [37] . Bacteria that reside in pathogen-modified vacuoles, such as Legionella pneumophila, Salmonella Typhimurium, and Mycobacterium tuberculosis, have also been reported to stimulate autophagy, also as measured by the above mentioned techniques [18, [38] [39] [40] [41] [42] . In both groups of bacteria that induce autophagy, it remains unclear if cytosolic translocation of bacteria and/or bacterial products, and/or phagosomal membrane damage, is the signal that induces autophagy. It is formally possible that all three induce autophagy under some conditions. In Drosophila, autophagy is induced by cytoplasmic peptidoglycan sensors, and the signaling pathway involved is independent of the known pathways that induce the expression of antimicrobial peptides [43] . Thus it is possible that L. monocytogenes induction of autophagy is multi-step process, with LLO falling upstream of an as-yet-unidentified receptor. However, the data presented here, with LLO-containing liposomes indicate that, while these other putative steps may play a role during bacterial infection, the presence of damaged membranes alone is sufficient to induce LC3 colocalization. The role of autophagy, if any, during L. monocytogenes infection is only just beginning to be appreciated. Previous studies have provided evidence that L. monocytogenes triggers autophagy, and that autophagy limits bacterial replication [23, 24, 43] . Further, bacterial mutants lacking the pore-forming cytolysin LLO fail to trigger autophagy [23, 24] . Zhao et al. (2008) recently reported that infection of mice lacking Atg5 in macrophages and neutrophils exhibited a modest increase in L. monocytogenes susceptibility.