Interactions of Salmonella with animals and plants

Abstract

Salmonella enterica species are Gram-negative bacteria, which are responsible for a wide range of food- and water-borne diseases in both humans and animals, thereby posing a major threat to public health. Recently, there has been an increasing number of reports, linking Salmonella contaminated raw vegetables and fruits with food poisoning. Many studies have shown that an essential feature of the pathogenicity of Salmonella is its capacity to cross a number of barriers requiring invasion of a large variety of cells and that the extent of internalization may be influenced by numerous factors. However, it is poorly understood how Salmonella successfully infects hosts as diversified as animals or plants. The aim of this review is to describe the different stages required for Salmonella interaction with its hosts: (i) attachment to host surfaces; (ii) entry processes; (iii) multiplication; (iv) suppression of host defense mechanisms; and to point out similarities and differences between animal and plant infections.

Keywords: Salmonella infections; adhesion; host defense strategies; invasion mechanisms; multiplication.

FIGURE 1

Transmission electron microscopy image showing fimbriae of S. Enteritidis after culture on Sven Gard plates. Bar represents 0.5 μm.

FIGURE 2

Models of Salmonella invasion mechanisms. Salmonella uses T3SS-1 to translocate effector proteins directly into host cells (left side; Bar of the transmission electron microscopy image represents 2 μm). Several of these effector proteins modulate host cell actin cytoskeleton, leading to an intense membrane ruffling and internalization of the bacteria into a modified phagosome or Salmonella-containing-vacuole (SCV). Salmonella can also invade cells via a T3SS-1-independent mechanism, which is induced by the Salmonella Rck membrane protein interacting with its receptor on the host cell plasma membrane and characterized by the induction of thin membrane extensions (right side; Bar of the transmission electron microscopy picture represents 1 μm). The membrane rearrangements induced by the Salmonella invasin PagN have not been studied yet.

FIGURE 3

Host cell markers present on the SCV (left) or on a phagosome (right). Comparison of the host cell markers, which characterize the classic endosome process and the biogenesis and maturation of the SCV (Figure modified from Bakowski et al., 2008).

FIGURE 4

Different behaviors of internalized Salmonella. The majority of Salmonella strains, internalized within an animal cell by the Trigger mechanism mediated by the T3SS-1, are enclosed in a canonical SCV where they can multiply, and form SIF, which allow delivery of nutrients. However, in some cases the bacteria do not have the time (or the capability) to modify the vacuole leading to the fusion of the SCV with phago-lysosome triggering intra-vacuole destruction or autophagy. In other cases, Salmonella damages the SCV membrane triggering vacuole destruction, allowing bacteria to escape into the cytosol, where they can be destroyed, particularly in activated macrophages, or multiply extensively especially in epithelial cells. No data have been obtained for the Zipper mechanism induced by Rck.