Abstract
Salmonella enterica is a species of bacteria that is a major cause of enteritis across the globe, while certain serovars cause typhoid, a more serious disease associated with a significant mortality rate. Type III secreted effectors are major contributors to the pathogenesis of Salmonella infections. Genes encoding effectors are acquired via horizontal gene transfer, and a subset are encoded within active phage lysogens. Because the acquisition of effectors is in flux, the complement of effectors possessed by various Salmonella strains frequently differs. By comparing the genome sequences of S. enterica serovar Typhimurium strain SL1344 with LT2, we identified a gene with significant similarity to SseK/NleB type III secreted effector proteins within a phage ST64B lysogen that is absent from LT2. We have named this gene sseK3. SseK3 was co-regulated with the SPI-2 type III secretion system in vitro and inside host cells, and was also injected into infected host cells. While no role for SseK3 in virulence could be identified, a role for the other family members in murine typhoid was found. SseK3 and other phage-encoded effectors were found to have a significant but sparse distribution in the available Salmonella genome sequences, indicating the potential for more uncharacterised effectors to be present in less studied serovars. These phage-encoded effectors may be principle subjects of contemporary selective processes shaping Salmonella-host interactions.
Highlights
Salmonella enterica is a Gram-negative intracellular bacterial pathogen of animals
The pathogenesis of Salmonella induced enteritis involves penetration of the intestinal epithelium and, through interactions with epithelial and immune cells, Salmonella induces significant inflammation in the intestine resulting in diarrhoea [1]
Relying on the hypothesis that the genetic complement of effectors frequently varies between strains, we aimed to identify novel effectors based on their similarity to known effectors by comparing the unannotated genome sequence of SL1344 to the
Summary
Salmonella enterica is a Gram-negative intracellular bacterial pathogen of animals. Salmonella is a major cause of enteritis across the world and is the cause of typhoid, a frequently fatal disease prevalent in developing nations. During typhoid, following penetration of the intestinal epithelium Salmonella enters phagocytic cells and is transported to the mesenteric lymph nodes and to the liver and spleen [1]. At these sites Salmonella resides primarily within macrophages and initiates substantial inflammation [2,3]. T3SS-1 and T3SS-2 (encoded by Salmonella pathogenicity islands 1 and 2, respectively) translocate effectors that collectively mediate penetration of the intestinal epithelium (T3SS-1) [5] or replication within phagocytic cells (T3SS-2) [6,7]. Effectors are hypothesized to interact with specific host molecules, which are subverted in order to benefit the infecting Salmonella [1]
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