Figure 1

Figure 1. From: Salmonella takes control: effector-driven manipulation of the host.

Schematic representation of the major stages underlying Salmonella infection. Salmonellae invade non-phagocytic cells by inducing membrane deformation and rearrangement of the underlying actin cytoskeleton (membrane ruffling), enclosing bacteria in intracellular phagosomal compartments termed Salmonella-containing vacuoles (SCVs). SCVs traffic towards the perinuclear region of the host cell and mature via selective interactions with the endocytic pathway. Once the SCV is positioned next to the Golgi apparatus, intracellular bacterial replication begins. This stage is characterised by the formation of SCV tubulovesicular structures called Salmonella-induced filaments (Sifs) and the accumulation of F-actin around the bacterial phagosome (actin nest). Chloride ion (Cl-) secretion and polymorphonuclear leukocyte (PMN) transmigration contribute towards diarrhoea and intestinal inflammation. In addition, Salmonella manipulates specific host immune response pathways. Salmonella serovars associated with systemic disease are able to enter intestinal macrophages, inducing cell death as well as using them as a vehicle to disseminate to the liver and spleen via the bloodstream and lymphatic system. SPI-1 and SPI-2 effectors involved in each individual infection stage are indicated. Note that SPI-1 and SPI-2 effectors do not operate sequentially and independently of one another as previously thought. Instead, both subsets play key roles in SCV maturation, positioning and replication (Abbreviations: ER, endoplasmic reticulum; TGN, trans-Golgi network).

Emma J McGhie, et al. Curr Opin Microbiol. 2009 February;12(1):117-124.

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