The pathogenicity island 1-encoded small RNA InvR mediates post-transcriptional feedback control of the activator HilA in .

Pathogenicity Island 1 (SPI1) encodes a type three secretion system (T3SS) essential for invasion of intestinal epithelial cells. Many environmental and regulatory signals control SPI1 gene expression, but in most cases, the molecular mechanisms remain unclear. Many of these regulatory signals control SPI1 at a post-transcriptional level and we have identified a number of small RNAs (sRNAs) that control the SPI1 regulatory circuit.

TamAB is regulated by PhoPQ and functions in outer membrane homeostasis during pathogenesis.

survive and replicate in macrophages, which normally kill bacteria by exposing them to a variety of harsh conditions and antimicrobial effectors, many of which target the bacterial cell envelope. The PhoPQ two-component system responds to the phagosome environment and induces factors that protect the outer membrane, allowing adaptation and growth in the macrophage. We show that PhoPQ induces the transcription of the operon both and in macrophages.

Cation Homeostasis: Coordinate Regulation of Polyamine and Magnesium Levels in Salmonella.

Polyamines are organic cations that are important in all domains of life. Here, we show that in Salmonella, polyamine levels and Mg levels are coordinately regulated and that this regulation is critical for viability under both low and high concentrations of polyamines. Upon Mg starvation, polyamine synthesis is induced, as is the production of the high-affinity Mg transporters MgtA and MgtB.

The Small RNA MicC Downregulates Translation To Control the Salmonella Pathogenicity Island 1 Type III Secretion System in Salmonella enterica Serovar Typhimurium.

Salmonella enterica serovar Typhimurium invades the intestinal epithelium and induces inflammatory diarrhea using the Salmonella pathogenicity island 1 (SPI1) type III secretion system (T3SS). Expression of the SPI1 T3SS is controlled by three AraC-like regulators, HilD, HilC, and RtsA, which form a feed-forward regulatory loop that leads to activation of , encoding the main transcriptional regulator of the T3SS structural genes. This complex system is affected by numerous regulatory proteins and environmental signals, many of which act at the level of mRNA translation or HilD protein function.

Long-Distance Effects of H-NS Binding in the Control of Expression in the Salmonella SPI1 Locus.

Salmonella enterica serovar Typhimurium utilizes a type three secretion system (T3SS) carried on the Salmonella pathogenicity island 1 (SPI1) to invade intestinal epithelial cells and induce inflammatory diarrhea. HilA activates expression of the T3SS structural genes. Expression of yper nvasion ocus A () is controlled by the transcription factors HilD, HilC, and RtsA, which act in a complex feed-forward regulatory loop.

HilE is required for synergistic activation of SPI-1 gene expression in Salmonella enterica serovar Typhimurium.

Background: Salmonella enterica serovar Typhimurium is an intestinal pathogen capable of infecting a wide range of animals. It initiates infection by invading intestinal epithelial cells using a type III secretion system encoded within Salmonella pathogenicity island 1 (SPI-1). The SPI-1 genes are regulated by multiple interacting transcription factors.

HilD, HilC, and RtsA Form Homodimers and Heterodimers To Regulate Expression of the Pathogenicity Island I Type III Secretion System.

serovar Typhimurium colonizes and invades host intestinal epithelial cells using the type three secretion system (T3SS) encoded on pathogenicity island 1 (SPI1). The level of SPI1 T3SS gene expression is controlled by the transcriptional activator HilA, encoded on SPI1. Expression of is positively regulated by three homologous transcriptional regulators, HilD, HilC, and RtsA, belonging to the AraC/XylS family.

Metal-independent variants of phosphoglycerate mutase promote resistance to nutritional immunity and retention of glycolysis during infection.

The ability of Staphylococcus aureus and other pathogens to consume glucose is critical during infection. However, glucose consumption increases the cellular demand for manganese sensitizing S. aureus to host-imposed manganese starvation.

PhoP-Mediated Repression of the SPI1 Type 3 Secretion System in Salmonella enterica Serovar Typhimurium.

must rapidly adapt to various niches in the host during infection. Relevant virulence factors must be appropriately induced, and systems that are detrimental in a particular environment must be turned off. infects intestinal epithelial cells using a type 3 secretion system (T3SS) encoded on pathogenicity island 1 (SPI1).

Controlled Activity of the Invasion-Associated Injectisome Reveals Its Intracellular Role in the Cytosolic Population.

The invasion-associated type III secretion system (T3SS1) is an essential virulence factor required for entry into nonphagocytic cells and consequent uptake into a -containing vacuole (SCV). While is typically regarded as a vacuolar pathogen, a subset of bacteria escape from the SCV in epithelial cells and eventually hyperreplicate in the cytosol. T3SS1 is downregulated following bacterial entry into mammalian cells, but cytosolic cells are T3SS1 induced, suggesting prolonged or resurgent activity of T3SS1 in this population.

Cytoplasmic Copper Detoxification in Salmonella Can Contribute to SodC Metalation but Is Dispensable during Systemic Infection.

serovar Typhimurium is a leading cause of foodborne disease worldwide. Severe infections result from the ability of Typhimurium to survive within host immune cells, despite being exposed to various host antimicrobial factors. SodCI, a copper-zinc-cofactored superoxide dismutase, is required to defend against phagocytic superoxide.

Mechanisms of Salmonella pathogenesis in animal models.

Animal models play an important role in understanding the mechanisms of bacterial pathogenesis. Here we review recent studies of infection in various animal models. Although mice are a classic animal model for , mice do not normally get diarrhea, raising the question of how well the model represents normal human infection.

Phagocyte roulette in Salmonella killing.

Salmonella propagates in macrophages to cause life-threatening infections, but the role of neutrophils in combating Salmonella has been controversial. In this issue, Burton et al. (2014) use single cell analyses and modeling to explain the ability of Salmonella to survive in macrophages while being killed by neutrophils.

Twin-arginine translocation system (tat) mutants of Salmonella are attenuated due to envelope defects, not respiratory defects.

The twin-arginine translocation system (Tat) transports folded proteins across the cytoplasmic membrane and is critical to virulence in Salmonella and other pathogens. Experimental and bioinformatic data indicate that 30 proteins are exported via Tat in Salmonella Typhimurium. However, there are no data linking specific Tat substrates with virulence.