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Journal of Biochemistry 2006 140(2):161-166; doi:10.1093/jb/mvj162
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© 2006 The Japanese Biochemical Society.

JB Minireview--Membrane Traffic in Physiology and Pathology

Autophagy in Innate Immunity against Intracellular Bacteria

Atsuo Amano1,4,*, Ichiro Nakagawa2,4 and Tamotsu Yoshimori3,4

1 Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, Suita-Osaka; 2 Division of Bacteriology, Department of Infectious Disease Control, International Research Center for Infectious Diseases, The Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo;3 Department of Cellular Regulation, Division of Cellular and Molecular Biology, Research Institute for Microbial Diseases, Osaka University, Suita-Osaka; and 4 PRESTO and CREST, Japan Science and Technology Agency, Kawaguchi 332-0012

* To whom correspondence should be addressed to: Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita-Osaka 565-0871. Tel: +81-6-6879-2976, Fax: +81-6-6876-8455, E-mail: amanoa{at}dent.osaka-u.ac.jp

Many pathogenic bacteria can invade phagocytic and non-phagocytic cells and colonize them intracellularly, then become disseminated to other cells. The endocytic degradation pathway is thought to be the only prevention against such intracellular pathogens. Autophagy, a fundamental cellular homeostasis pathway that operates with the intracellular degradation/recycling system, causes the turnover of cellular components by delivering portions of the cytoplasm and organelles to lysosomes. Recently, we reported that autophagic degradation is a previously unrecognized effector of host innate immunity. Streptococcus pyogenes (Group A Streptococcus; GAS) successfully enters human epithelial cells via endocytosis. GAS immediately escapes from the endosomes to the cytoplasm and gains a replicative niche, after which GAS in the cytoplasm is trapped in autophagosome-like compartments and degraded upon fusion with lysosomes. This process indicates that autophagy plays a protective role in infectious diseases. We also found that autophagic degradation was induced against Staphylococcus aureus, while methicillin-resistant S. aureus were resistant to autophagic degradation. The present review focuses on the protective function of autophagy against bacterial invasion of cells.


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