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Intracellular survival of Shigella Ogawa M; Sasakawa CCell Microbiol 2006[Feb]; 8 (2): 177-84Bacterial invasion of eukaryotic cells and host recognition and killing of the invading bacteria are a key issue in determining the fate of bacterial infection. Once inside host cells, pathogenic bacteria often modify the phagosomal compartment or enter the host cytosol to escape from the lytic compartment and gain a replicative niche. Cytosolic invaders, however, are monitored by host innate immune systems, such as mediated by Nod/CARD family proteins, which induce inflammatory responses via activation of NF-kappaB. Furthermore, recent studies indicate that autophagy, a major cytoplasmic degradation system that eliminates cytosolic protein and organelles, also recognizes invading bacteria. Indeed, unless they are able to circumvent entrapping by autophagic membranes, bacteria targeted by autophagy ultimately undergo degradation by delivery into autolysosomes. In this article, we review recent advances in understanding of Shigella strategies to infect epithelial cells, and then focus on recent studies of an intriguing bacterial survival strategy against autophagic degradation.|*Microbial Viability[MESH]|Animals[MESH]|Autophagy[MESH]|Bacterial Proteins/physiology[MESH]|Cytoplasm/metabolism[MESH]|Epithelial Cells/microbiology[MESH]|Gram-Negative Bacterial Infections/metabolism/microbiology[MESH]|Humans[MESH]|Immunity, Cellular[MESH]|Immunity, Innate[MESH]|Intestinal Mucosa/microbiology[MESH]|Intracellular Membranes/metabolism[MESH]|Macrophages/microbiology[MESH]|NF-kappa B/metabolism[MESH]|Shigella/*physiology[MESH] |
