Autophagy Controls Salmonella Infection in Response to Damage to the Salmonella-containing Vacuole

摘要: Salmonella enterica serovar Typhimurium (S. Typhimurium) is a facultative intracellular pathogen that causes disease in variety of hosts. S. actively invade host cells and typically reside within membrane-bound compartment called the Salmonella-containing vacuole (SCV). The bacteria modify fate SCV using two independent type III secretion systems (TTSS). TTSS are known to damage eukaryotic cell membranes has been suggested its pathogenicity island (SPI)-1 encoded TTSS. Here we show this gives rise an bacterial population targeted by autophagy system during vitro infection. Approximately 20% colocalized with marker GFP-LC3 at 1 h postinfection. Autophagy was dependent upon SPI-1 protein synthesis. Bacteria were often associated ubiquitinated proteins, indicating their exposure cytosol. Surprisingly, these also markers. Autophagy-deficient (atg5-/-) more permissive for growth than normal cells, allowing increased We propose model which targets SCVs damaged This serves retain vacuoles early after infection protect cytosol from colonization. Our findings support role innate immunity demonstrate powerful study process.