Salmonella Pathogenicity Island 1(SPI-1) at Work

Abstract

As an indispensable virulence determinant, Salmonella pathogenicity island 1(SPI-1) has gained much attention in host-pathogen interactions. More and more studies on SPI-1 have demonstrated that it is far more complex than the one we used to expect. It not only affects sophisticated activities during infection, including invasion, replication, and host responses, but also extends to other fields like biofilm formation. In addition, mutants in SPI-1 effectors have been explored as vaccines, the effective ways to prevent salmonellosis. The activity of SPI-1 is influenced by many factors which have been widely reported. Investigations on these factors may provide new insights into prevention and treatment of salmonellosis. Therefore, SPI-1 is a tempting issue worthy of further exploration. In this review, we will probe into SPI-1 systematically.

Age-Dependent Enterocyte Invasion and Microcolony Formation by Salmonella

“…Invasion of non-phagocytic epithelial cells is facilitated by virulence factors encoded by the pathogenicity island SPI1 [6]. The critical role of SPI1 for enteric disease is illustrated by its presence in all subspecies of Salmonella enterica [33] and its high prevalence in clinical Salmonella isolates [9].…”

“…SPI1 encodes a type III secretion systems (T3SS) and a set of effector molecules that are translocated into the target cell. It mediates pathogen-induced internalization in non-phagocytic cells [6]–[8]. The critical importance of cellular invasion by Salmonella and intracellular proliferation in non-phagocytic cells is supported by epidemiological data and has been extensively studied in vitro [6], [9]–[10].…”

“…It mediates pathogen-induced internalization in non-phagocytic cells [6]–[8]. The critical importance of cellular invasion by Salmonella and intracellular proliferation in non-phagocytic cells is supported by epidemiological data and has been extensively studied in vitro [6], [9]–[10]. Although intracellular Salmonella have been observed in epithelial cells and cells of the lamina propria also in vivo , this host cell interaction and the functional importance have remained less defined [7]–[8], [11]–[15].…”

Interferon-γ in Salmonella pathogenesis: New tricks for an old dog

“…Invasion of intestinal epithelial cells is mediated by a chromosomal genetic island called Salmonella Pathogenicity-Island 1 (SPI-1) 13–16 . SPI-1 encodes a Type III secretion system (T3SS) that injects dozens of effector proteins into the cytosol of epithelial cells 17 . A subset of these effectors, most notably the Sop proteins SopB, SopE, and SopE2, remodel host actin, allowing ingress of Salmonella into the host cytosol 18–21 .…”

Bacterial Genome Instability

“…Introduction of a new GI can result in a total change of phenotype, behavior, or life-style of the receiving organism. Depending on the provided phenotypic advantages, a GI can be a pathogenicity island (such as Salmonella pathogenicity island 1 [SPI1] [104]), a fitness island (such as E. coli acid fitness island [AFI] [105]), a metabolic island (such as the Xanthomonas xanthan gum production island [106]), a resistance island (to antibiotics) (such as AbaR7 in Acinetobacter baumannii [107]), a symbiosis island (such as the Mesorhizobium loti strain R7A symbiosis island [108]), a saprophytic island (like the island encoding adhesins in some E. coli strains [94]), an ecological island (such as an island permitting phenol degradation in Pseudomonas putida [94,109]), or a defense island (as in Shewanella sp. strain ANA-3 [110]).…”