Remodelling of the actin cytoskeleton is essential for replication of intravacuolar Salmonella

Cell Microbiol. 2001 Aug;3(8):567-77. doi: 10.1046/j.1462-5822.2001.00141.x.


Maturation and maintenance of the intracellular vacuole in which Salmonella replicates is controlled by virulence proteins including the type III secretion system encoded by Salmonella pathogenicity island 2 (SPI-2). Here, we show that, several hours after bacterial uptake into different host cell types, Salmonella induces the formation of an F-actin meshwork around bacterial vacuoles. This structure is assembled de novo from the cellular G-actin pool in close proximity to the Salmonella vacuolar membrane. We demonstrate that the phenomenon does not require the Inv/Spa type III secretion system or cognate effector proteins, which induce actin polymerization during bacterial invasion, but does require a functional SPI-2 type III secretion system, which plays an important role in intracellular replication and systemic infection in mice. Treatment with actin-depolymerizing agents significantly inhibited intramacrophage replication of wild-type Salmonella typhimurium. Furthermore, after this treatment, wild-type bacteria were released into the host cell cytoplasm, whereas SPI-2 mutant bacteria remained within vacuoles. We conclude that actin assembly plays an important role in the establishment of an intracellular niche that sustains bacterial growth.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism*
  • Animals
  • Cell Division
  • Cytoskeleton / metabolism*
  • Macrophages, Peritoneal / microbiology
  • Mice
  • Mice, Inbred BALB C
  • Salmonella typhimurium / cytology
  • Salmonella typhimurium / pathogenicity*
  • Vacuoles / microbiology*


  • Actins