In the case of Salmonella, some serovars have accumulated mutations that enhance their survival within their respective hosts. For example the poultry-adapted S. Pullorum and S. Gallinarum serovars are non-motile because they have a point mutation in the flgK gene [11, 12]. When S. Enteritidis and S. Staurosporine Typhimurium are isolated from infected poultry, these bacteria are frequently non-motile, suggesting that the niche occupied in birds can select against flagellation [13]. These non-motile S. Typhimurium strains have been shown to be non-virulent when

used to infect mice. Thus, in the S. enterica, the adaptation to a particular vertebrate host seems to drive the loss of virulence factors for some serovars. The result of this adaptation may contribute to the narrowing of the host range and to the development of host specificity [14]. S. Typhi is an intracellular facultative pathogen that contains over 200 pseudogenes, AZD1152 nmr nearly 5% of its whole genome Compound C datasheet [15, 16]. Several of the mutations that gave rise to these pseudogenes occur in systems related to pathogenicity mechanisms. For example, the S. Typhimurium sseJ gene encodes an effector protein regulated by Salmonella pathogenicity

island 2 (SPI-2) [17, 18]. SPI-2 regulated genes are related to bacterial intracellular trafficking and proliferation, and encode a protein complex known as the type III secretion system (T3SS). The T3SS mediates the injection of effector proteins from bacteria into eukaryotic cells [19–21]. These effector proteins modulate the S. Typhimurium endocytic pathway and allow the establishment of bacteria in a specialised vacuole termed the Salmonella-containing vacuole (SCV) [22]. Late stages of SCV synthesis include the formation of tubular membrane extensions next known as Salmonella-induced filaments (Sifs).

Sifs are thought to result from the fusion of late endocytic compartments with the SCV and their formation requires at least five SPI-2-dependent effectors: SifA, SseF, SseG, SopD2 and SseJ [23–26]. In this context, S. Typhimurium sseJ encodes an acyltransferase/lipase that participates in SCV biogenesis in human epithelial cell lines [25, 27–29]. The coordination of SseJ and SifA is required for bacterial intracellular proliferation [30]. Some studies have shown that SseJ is needed for full virulence of S. Typhimurium in mice and for proliferation within human culture cells [31]. S. Typhi lacks several effector proteins that are crucial for the pathogenicity of the generalist serovar S. Typhimurium [29]. The absence of these proteins could contribute to the specificity of the human-restricted serovars, and could play a role in evolutionary adaptation. In S. Typhi, sseJ is considered a pseudogene. In this work, we studied the effect of trans-complementing S. Typhi with the S. Typhimurium sseJ gene and assessed the phenotype in human cell lines.