2017 年 67 巻 2-4 号 p. 115-128
Autophagy, a cellular homeostatic pathway, is emerged as an innate immune response against intracellular pathogens. It can directly eliminate invading bacteria by mediating their delivery to lysosomes. However, successful intracellular pathogens have developed mechanism(s) to escape or subvert autophagy for their intracellular niches. Studies on interplay between autophagy and intracellular pathogens are very important for understanding how infections occur. Particularly, Staphylococcus aureus is an important opportunistic pathogen that causes a wide range of infections. Classically, S. aureus is considered as an extracellular pathogen, but cumulative evidence indicates that this bacterium invades epithelial cells and replicates intracellularly which is relevant to intracellular persistence and chronic infections. A serious therapeutic problem of staphylococcal infections is caused by antibiotic resistant strains which have emerged increasingly in recent years. Thus, new insights in the strategy of S. aureus to interplay with autophagy is urgently required. This review highlights an impact of S. aureus toxins on autophagy. Alpha-hemolysin activates autophagy and prevents lysosome-autophagosome fusion, whereas toxic shock syndrome toxin-1 suppresses autophagosome formation. This opposite function indicates a complicated relationship between autophagy and intracellular adaptation of S. aureus. The possible effects of these toxins on S. aureus infections are also addressed in this review.