Modification of host cells by intracellular Salmonella

Salmonella enterica is a facultative intracellular pathogen that resides in a unique membrane-bound compartment, referred to as Salmonella-containing vacuole or SCV. Within the SCV, Salmonella is able to survive the antimicrobial activities of phagocytic cells and can rapidly multiply in a variety of host cells. Intracellular life of Salmonella is dependent on a large number of virulence traits, but the function of the type III secretion system (T3SS) encoded by Salmonella Pathogenicity Island 2 (SPI2) is of central importance. Image "SIF.jpg"
HeLa cells were infected with Salmonella wild type or a SPI2-deficient strain. Cells were fixed 16 after infection the immunostaining for the bacteria (green) and the host cell endosomal marker LAMP1 (red) was performed. Infection with wild-type Salmonella induced the formation of extensive tubular aggregates of endosomes (arrowheads).
Although more than 20 effector proteins have been identified as translocated by the SPI2-T3SS, the molecular function and contribution to intracellular live is only known for a few of these proteins. Intracellular Salmonella modify basic functions of the host cell such as the structure of the microtubule cytoskeleton and induce a massive reorganization of vesicular transport and the endosomal system. Unique phenomena are the SPI2-dependent induction of extensive tubular membrane aggregations of endosomal or Golgi-derived vesicles. The SCV itself has features of a novel organelle and the fate of this compartment is controlled by the pathogen. Previous observations indicated that the SCV is arrested in the state of late endosomal compartment, but recent studies using advanced ultrastructural analyses and live cell studies indicate a complex and highly dynamic interaction of the intracellular Salmonella and their host cells.

We aim to

  • define the role of individual SPI2-T3SS effectors in modification of cellular transport and remodeling of the endosomal system
  • characterize host factors involved in remodeling of the endosomal system by Salmonella
  • identify interaction partners of effectors by genetic screens and protein interaction analyses
  • determine the structure function-relationship of SPI2-T3SS effectors.

The identification and analyses of effector/target interactions in the proposed project will lead to a molecular understanding of the intracellular strategies of an important intracellular pathogen.


The project is currently funded by the DFG, project HE1964/17-1


  • Prof. Dr. Yves Muller, FAU Erlangen-Nürnberg
  • Prof. Dr. Dipa Chakravortty, Indian Institute of Science, Bangalore, Indien

Original papers:

Rajashekar, R., Liebl, D., Seitz, A., and Hensel, M. (2008). Dynamic remodeling of the endosomal system during formation of Salmonella-induced filaments by intracellular Salmonella enterica. Traffic 9, 2100-2116.
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Kuhle, V., Abrahams, G.L., and Hensel, M. (2006). Intracellular Salmonella enterica redirect exocytic transport processes in a Salmonella pathogenicity island 2-dependent manner. Traffic 7, 716-730.

Chakravortty, D., Rohde, M., Jäger, L., Deiwick, J., and Hensel, M. (2005). Formation of a novel surface structure encoded by Salmonella Pathogenicity Island 2. EMBO J 24, 2043-2052.


Abrahams, G.L., and Hensel, M. (2006). Manipulating cellular transport and immune responses: dynamic interactions between intracellular Salmonella enterica and its host cells. Cell Microbiol 8, 728-737.

Kuhle, V., and Hensel, M. (2004). Cellular microbiology of intracellular Salmonella enterica: functions of the type III secretion system encoded by Salmonella pathogenicity island 2. Cell Mol Life Sci 61, 2812-2826.
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