he highly virulent Francisella tularensis proliferates in a wide range of phagocytic and non-phagocytic host cells and induces host cell death in macrophages. Although its genome recently was sequenced [Nature Genetics 37(2005)153], most of the factors allowing its intracellular replication still remain elusive. Another obstacle is the lack of genetic systems. There are three important recent discoveries regarding the features of cells infected with F. tularensis. i) Host cells are incapable of secreting proinflammatory cytopkines [Cell. Microbiol. 5(2003)41]. ii) F. tularensis rapidly escapes into the phagosome after uptake [Infect. Immun. 71(2003)5940]. iii) Monocytic cells eventually undergo apoptosis after infection [Infect. Immun. 71(2003)4642]. Moreover, we have established a model for F. tularensis in Drosophila melanogaster. Using this model, the iglC mutant is attenuated for virulence
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PI: Anders Sjöstedt
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