pathways and inflammatory responses, suggesting a link between autophagy and cellular inflammation (Chang et al., 2010). Antimicrobial peptides are major components of the bactericidal machinery of mammalian phagocytes, and play an important role as innate effectors during bacterial and viral infections (Cederlund et al., 2011). Of the antimicrobial peptides, cathelicidins exert antimicrobial activities against mycobacteria (Liu et al., 2006; Yang et al., 2009; Sonawane et al., 2011). Interestingly, vitamin D activates anti- mycobacterial autophagy through induction of cathelicidin, which contributes to the promoter activation of the autophagy-related genes Atg5 and Beclin-1, as well as co-localization of bacterial phagosomes and autophagosomes (Yuk et al., 2009b). Future studies are necessary to fully elucidate the roles of the numerous antimicrobial peptides in the context of autophagy activation leading to collaboration with innate immunity. Bacterial tactics to modulate host autophagy Intracellular bacterial pathogens have developed multiple strategies for exploiting or hijacking eu- karyotic functions in order to survive and multiply inside host cells (Knodler et al., 2001). Consistently, numerous pathogens antagonize the initiation and maturation of autophagic processes, evade auto- phagic recognition, or hijack the autophagy pathway to facilitate intracellular survival or replication (Levine et al., 2011). The various strategies used by bacterial patho- gens are summarized in Figure 1. In this section, we will summarize two strategies by which bacterial pathogens can escape from or interact with auto- phagic pathways: 1) physical escape from de- gradative endocytic compartments and replication within the cytoplasm (Shigella, Listeria, Rickettsia); and 2) survival and replication within membrane- bound compartments (Mycobacteria, Salmonella, Francisella, Legionella, Brucella, Chlamydia, Por- phyromonas gingivalis). Bacterial escape into cytosol after breaking the host jail (bacterial endocytic compartments): Shigella, Rickettsia, M. marinum, and Listeria Intracellular bacteria such as Shigella flexneri and Listeria monocytogenes can evade autophagic recognition, survive, and replicate in phagocytic and non-phagocytic cells by disrupting vacuoles and escaping into the cytoplasm (Ogawa et al., 2005), and acquisition of actin-based motilities Autophagy in infectious diseases 103 (Cossart, 2000), respectively. S. flexneri can block autophagic targeting through the secreted T3SS effector icsB that competes with the autophagy protein Atg5 for binding to the S. flexneri surface protein VirG (Ogawa et al., 2005). Thus, icsB deletion mutants are not able to survive in host cells (Ogawa et al., 2005). When S. flexneri breaks the vacuolar membrane and escapes from the phagosome, the vacuolar membrane fragments are polyubiquitinated, and targeted to autophagic degradation through p62 accumulation on mem- brane remnants (Dupont et al., 2009). Rickettsia are Gram-negative obligate intracellular bacteria, and can be transmitted to humans via arthropod vectors (Azad and Beard, 1998). After infection, Rickettsia can escape from phagosomes into their eukaryotic host cytoplasm, where they replicate and infect adjacent cells (Silverman and Wisseman, 1979; Walker, 2007). Earlier studies reported that rickettsial infection of polymorphonuclear leukocytes results in autophagosome formation (Rikihisa, 1984). The detailed mechanisms by which Rickettsia are able to escape from autophagy machinery remain to be determined. Conversely, the host autophagy induced during rickettsial infection is recognized as an important defense mechanism against this invading pathogen (Walker, 2007; Deretic, 2010). One report indicated that Rickettsia-induced proinflammatory cytokines led to increased activation of the autophagy that is required for bacterial inhibition (Walker et al., 1997). Mycobacterium marinum, a natural pathogen, and the closest relative of M. tuberculosis with a homology of 99.4% (Stamm and Brown, 2004), has been shown to escape from the phagosome and enter the cytosol via an ESX-1-dependent mechanism (Collins et al., 2009). In the cytosol, some M. marinum promote motility through actin polymerization, while non-motile bacteria are decorated by ubiquitin and sequestered in the host Lamp1-positive vesicular compartments by autophagosome-like double mem- branes, formation of which is independent of Atg5 (Collins et al., 2009). L. monocytogenes can replicate in LAMP1-positive spacious Listeria-containing phagosomes (SLAPs), the formation of which is dependent on both the bacterial virulence toxin listeriolysin O and host autophagy (Birmingham et al., 2008). Interestingly, the listerial virulence factor actA triggers host protein recruitment and actin polymerization, which propels bacteria from one cell to another (Cossart, 2000) and prevents autophagic recognition of bacteria within the cytosol (Yoshikawa et al., 2009). L. monocytogenes expressing-actA mutants that cannot recruit host proteins for actin polymerization