Typhimurium remains an important concern to the poultry industry [8] causing a systemic infection in newly hatched chicks, often resulting in death [9]. In

older birds infection by Typhimurium leads to an asymptomatic carriage State with colonization of the digestive tract and continuous shedding [10, 11]. These healthy carrier birds constitute a risk of contamination Selonsertib molecular weight of newly hatched chickens, as well as the food chain leading to both important economic losses and potential harm to human consumers. The pathogenesis of Salmonella has been extensively studied in the mouse [12]. In susceptible mice, Salmonella causes an acute systemic disease with limited intestinal manifestations [13]. Recently, a model of Salmonella enterocolitis has been developed

in streptomycin-treated mice [14]. Studies using these mice and other animal models of Salmonella diseases have yielded substantial data about the molecular players involved at different levels. The Salmonella pathogeniCity islands (SPIs) 1 and 2 are two major virulence determinants of S. enterica. They encode type III secretion systems (T3SS) that form syringe-like organelles on the surface of gram-negative bacteria and enable the injection of effector proteins Staurosporine ic50 directly into the cytosol of eukaryotic cells [15, 16]. These effectors ultimately manipulate the cellular functions of the infected host and facilitate the progression of the infection. SPI1 and SPI2 play several roles in different organs within the host. SPI1 primarily promotes the invasion of non-phagocytic intestinal epithelial cells and the initiation of the inflammatory responses in the intestines [17, 18]. It is also involved in the survival and persistence of Salmonella in the systemic compartment of the host [19–21]. The first characterized role of

SPI2 was its PIK-5 ability to promote Salmonella survival and multiplication in phagocytic cells that constitute the main reservoirs for dissemination of the bacteria into systemic organs [16]. SPI2 also plays an important role in the intestinal phase of Salmonella infection in mice [17, 22, 23]. The regulation of SPI1 and SPI2 gene expression involves numerous transcriptional regulators located both inside and outside these pathogeniCity islands. The regulation of SPI1 is particularly complex. SPI1 encodes for the five regulators HilA, HilC, HilD, InvF, and SprB (Figure 1). The first four of which are involved in regulatory pathways that lead to the activation of SPI1 genes and of genes encoding T3SS effectors located outside SPI1. In contrast to SPI1 the regulation of SPI2 genes is simpler with the SsrAB two-component system being the only transcriptional regulator encoded within SPI2 that activates the expression of SPI2 genes and of genes encoding T3SS effectors located outside SPI2.