Abstract
Salmonella Typhimurium has a broad arsenal of genes that are tightly regulated and coordinated to facilitate adaptation to the various host environments it colonizes. The genome of Salmonella Typhimurium has undergone multiple gene acquisition events and has accrued changes in non-coding DNA that have undergone selection by regulatory evolution. Together, at least 17 horizontally acquired pathogenicity islands (SPIs), prophage-associated genes, and changes in core genome regulation contribute to the virulence program of Salmonella. Here, we review the latest understanding of these elements and their contributions to pathogenesis, emphasizing the regulatory circuitry that controls niche-specific gene expression. In addition to an overview of the importance of SPI-1 and SPI-2 to host invasion and colonization, we describe the recently characterized contributions of other SPIs, including the antibacterial activity of SPI-6 and adhesion and invasion mediated by SPI-4. We further discuss how these fitness traits have been integrated into the regulatory circuitry of the bacterial cell through cis-regulatory evolution and by a careful balance of silencing and counter-silencing by regulatory proteins. Detailed understanding of regulatory evolution within Salmonella is uncovering novel aspects of infection biology that relate to host-pathogen interactions and evasion of host immunity.
Highlights
Salmonella is a genus of enteric pathogens that consists of two species, Salmonella enterica and Salmonella bongori, which can cause disease in a broad range of hosts
In addition to an overview of the importance of Salmonella Pathogenicity Islands (SPIs)-1 and SPI-2 to host invasion and colonization, we describe the recently characterized contributions of other SPIs, including the antibacterial activity of SPI-6 and adhesion and invasion mediated by SPI-4
There are a number of core genes that contribute to pathogenesis, such as motility genes required for chemotaxis within the gut lumen, fimbrial adhesins involved in mediating host cell contact, and metabolic genes that allow for nutrient acquisition in the competitive anaerobic gut environment
Summary
Salmonella is a genus of enteric pathogens that consists of two species, Salmonella enterica and Salmonella bongori, which can cause disease in a broad range of hosts. One of the key mediators of this intestinal inflammation are the gene products of the Salmonella pathogenicity island 1 (SPI-1; Lee et al, 2000) This island encodes a type 3 secretion system (T3SS-1) that translocates effector proteins into host cells to modulate their function. The suite of horizontally acquired virulence genes found across the SPIs act in a concerted fashion to drive infection, as Salmonella successfully outcompetes the host microbiota, colonizes the lumen, invades the intestinal epithelium, and resides within the replicative niches of neutrophils and macrophages. H-NS binds to SPIs 1-6 as well as other virulence-associated
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