Salmonella proteome
Ontology highlight
ABSTRACT:
ORGANISM(S): Salmonella Enterica Subsp. Enterica Serovar Typhimurium Str. Lt2
SUBMITTER: 
Xiaoyun Liu
PROVIDER: PXD011191 | iProX | Wed Sep 26 00:00:00 BST 2018
REPOSITORIES: iProX
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 1000ng.raw | Raw | |||
| 1h-1-1.raw | Raw | |||
| 1h-1-2.raw | Raw | |||
| 1h-1-3.raw | Raw | |||
| 1h-2-1.raw | Raw |
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Project description:SrfJ is an effector of the type III secretion systems of the Gram-negative intracellular pathogen Salmonella enterica serovar Typhimurium. To study the effects of this effector on global gene expression in host cells, we have infected murine RAW264.7 macrophages with two strains of Salmonella enterica serovar Typhimurium. The comparison between cells infected with the wild-type strain and cells infected with a srfJ mutant revealed a number of genes that are differentially expressed when SrfJ is present.
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Project description:The speG gene has been reported to regulate polyamine metabolism in Escherichia coli and Shigella, but its role in Salmonella remains unknown. Our preliminary studies have revealed that speG widely affects the transcriptomes of infected in vitro M and Caco-2 cells and that it is required for the intracellular replication of Salmonella enterica serovar Typhimurium (S. Typhimurium) in HeLa cells. In this study, we demonstrated that speG plays a time-dependent and cell type-independent role in the intracellular replication of S. Typhimurium. Moreover, high-performance liquid chromatography of four major polyamines demonstrated putrescine, spermine, and cadaverine as the leading polyamines in S. Typhimurium. The deletion of speG significantly increased the levels of the three polyamines in intracellular S. Typhimurium, suggesting the inhibitory effect of speG on the biosynthesis of these polyamines. The deletion of speG was associated with elevated levels of these polyamines in the attenuated intracellular replication of S. Typhimurium in host cells, which was subsequently validated by the dose-dependent suppression of intracellular proliferation after the addition of the polyamines. Furthermore, our RNA transcriptome analysis of S. Typhimurium SL1344 and its speG mutant outside and inside Caco-2 cells revealed that speG regulates the genes with documented virulence in flagellar biosynthesis, fimbrial expression, and functions of types III and I secretion systems. speG also affects the expression of genes that have been rarely reported to correlate with polyamine metabolism, including those associated with the periplasmic nitrate reductase system, glucarate metabolism, the phosphotransferase system, cytochromes, and the succinate reductase complex in S. Typhimurium in the mid-log growth phase, as well as those in the ilv–leu and histidine operons of intracellular S. Typhimurium after invasion in Caco-2 cells. In the present study, we characterized the phenotypes and transcriptome effects of speG in S. Typhimurium and reviewed the relevant literature to facilitate a more comprehensive understanding of the key role of speG in the polyamine metabolism and virulence regulation of Salmonella.
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Project description:<p><em>Salmonella Typhimurium</em> establishes systemic infection by replicating in host macrophages. Here we show that macrophages infected with <em>S. Typhimurium</em> exhibit upregulated glycolysis and decreased serine synthesis, leading to accumulation of glycolytic intermediates. The effects on serine synthesis are mediated by bacterial protein SopE2, a type III secretion system (T3SS) effector encoded in pathogenicity island SPI-1. The changes in host metabolism promote intracellular replication of <em>S. Typhimurium</em> via two mechanisms: decreased glucose levels lead to upregulated bacterial uptake of 2- and 3-phosphoglycerate and phosphoenolpyruvate (carbon sources), while increased pyruvate and lactate levels induce upregulation of another pathogenicity island, SPI-2, known to encode virulence factors. Pharmacological or genetic inhibition of host glycolysis, activation of host serine synthesis, or deletion of either the bacterial transport or signal sensor systems for those host glycolytic intermediates impairs <em>S. Typhimurium</em> replication or virulence.</p>
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Project description:SrfJ is an effector of the type III secretion systems of the Gram-negative intracellular pathogen Salmonella enterica serovar Typhimurium. To study the effects of this effector on global gene expression in host cells, we have expressed SrfJ on human HeLa cells through transient transfection. The comparison with HeLa cells transfected with a plasmid not expressing SrfJ, revealed a number of genes that are differentially expressed when SrfJ is present.
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Project description:Bacterial pathogens adapt to multiple stress conditions; however, the consequences of these responses on infection are not well understood. Here, the adaptive responses of Salmonella enterica serovar Typhimurium (S. typhimurium) to the combination of nutritional deprivation and high temperature (NDHT) stress were investigated. Microarray analysis revealed extensive modulation of expression of genes involved in several metabolic pathways. Interestingly, the expression of a large number of genes involved in chemotaxis, invasion, motility etc are down regulated. Further studies involved S. typhimurium exposed to high temperature (HT) or grown in minimal media, i.e. nutritional downshift (ND), or the combination, i.e. NDHT. The amounts of secretory proteins reduce greatly during NDHT, but not ND or HT, resulting in lower number of colony forming units (CFU) in different organs post oral infection of mice. The expression of the global regulator, RpoS, is downregulated during NDHT. Deletion of rpoS greatly reduces the amounts of secretory proteins and intracellular replication of S. typhimurium during ND but not HT. Extension of these results to RAW macrophage cells demonstrated lower intracellular replication of S. typhimurium at HT. Overall, this study sheds insights on the adaptive responses of S. typhimurium to a combination of stress conditions, resulting in lower infection. Agilent one-color experiment,Organism: Salmonella Typhimurium ,Agilent-Custom GeneExpression 8x15k designed by Genotypic Technology Pvt. Ltd. (AMADID: 017809) , Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
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Project description:Bacterial pathogens adapt to multiple stress conditions; however, the consequences of these responses on infection are not well understood. Here, the adaptive responses of Salmonella enterica serovar Typhimurium (S. typhimurium) to the combination of nutritional deprivation and high temperature (NDHT) stress were investigated. Microarray analysis revealed extensive modulation of expression of genes involved in several metabolic pathways. Interestingly, the expression of a large number of genes involved in chemotaxis, invasion, motility etc are down regulated. Further studies involved S. typhimurium exposed to high temperature (HT) or grown in minimal media, i.e. nutritional downshift (ND), or the combination, i.e. NDHT. The amounts of secretory proteins reduce greatly during NDHT, but not ND or HT, resulting in lower number of colony forming units (CFU) in different organs post oral infection of mice. The expression of the global regulator, RpoS, is downregulated during NDHT. Deletion of rpoS greatly reduces the amounts of secretory proteins and intracellular replication of S. typhimurium during ND but not HT. Extension of these results to RAW macrophage cells demonstrated lower intracellular replication of S. typhimurium at HT. Overall, this study sheds insights on the adaptive responses of S. typhimurium to a combination of stress conditions, resulting in lower infection.
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Project description:MicroRNAs have well-established roles in eukaryotic host responses to viruses and extracellular bacterial pathogens. In contrast, microRNA responses to invasive bacteria have remained unknown. Here, we report cell type-dependent microRNA regulations upon infection of mammalian cells with the enteroinvasive pathogen, Salmonella Typhimurium. Murine macrophages strongly up-regulate NF-κB associated microRNAs; strikingly, these regulations which are induced by the bacterial lipopolysaccharides (LPS) occur and persist regardless of successful host invasion and/or replication, or whether an inflammatory response is mounted, suggesting that microRNAs belong to the first line of anti-bacterial defence. However, a suppression of the global immune regulator miR-155 in endotoxintolerant macrophages revealed that microRNA responses also depend on the status of infected cells. This study identifies the let-7 family as the common denominator of Salmonella regulated microRNAs in macrophages and epithelial cells, and suggests that repression of let-7 relieves cytokine IL-6 and IL-10 mRNAs from negative post-transcriptional control. Our results establish a paradigm of microRNA-mediated feed-forward activation of inflammatory factors when mammalian cells are targeted by bacterial pathogens. The murine macrophage cell-line RAW 264.7 was exposed to wild-type Salmonella typhimurium SL1344 or to the corresponding knockout strain lacking both major genomic loci associated with Salmonella pathogenicity ("SPI1" and "SPI2"). To induce infectivity overnight cultures of Salmonella were dilluted 1:100 and grown to OD2. Host cells at a density of approximately 10e6 per well of a 6-well plate were infected at an MOI of 1. Upon initial incubation for 30 min cells were further incubated for 24 h in RPMI supplemented with gentamicin (10 µg / ml). As determined by a gentamicin protection and plating assay the SPI1/2 double knockout strain is deficient in both invasion and intracellular replication. We compared mouse mRNA abundances between cells infected with wild-type ("24WT") or SPI1/2 knockout Salmonella ("24SPI1/2") and non-infected, mock-treated controls ("24C"). Both strains mounted a similar inflammatory response as judged from the abundance of pro-inflammatory genes compared to the controls. These data indicate, that macrophages can mount a full inflammatory response to extracellular bacteria, that is not further enhanced or attenuated by the sensing of intracellular bacteria. Murine RAW 264.7 cells were rendered endotoxin-tolerant by pre-exposure to heat-killed Salmonella typhimurium SL1344 ("HKS") at an MOI of 10 for 20 h. 5 days upon removal of the HKS stimulus cells were exposed to wild-type Salmonella typhimurium SL1344 or to the corresponding knockout strain lacking both major genomic loci associated with Salmonella pathogenicity ("SPI1" and "SPI2"). To induce infectivity overnight cultures of Salmonella were dilluted 1:100 and grown to OD2. Host cells at a density of approximately 10e6 per well of a 6-well plate were infected at an MOI of 1. Upon initial incubation for 30 min cells were further incubated for 24 h in RPMI supplemented with gentamicin (10 µg / ml). As determined by a gentamicin protection and plating assay the SPI1/2 double knockout strain is deficient in both invasion and intracellular replication. The wild-type Salmonella strain invades and replicates in endotoxin-tolerant RAW 264.7 cells, though the intracellular replication rate is significantly reduced (by roughly 40 %) compared to naive RAW 264.7 cells. We compared mouse mRNA abundances between cells infected with wild-type ("wt") and non-infected, mock-treated controls ("Mock") or between wild-type ("wt") and SPI1/2-knockout ("SPI1/2") infected cells. As apparent from the Microarray data the wild-type Salmonella strain induces a typical inflamatory response in endotoxin-tolerant RAW 264.7 cells (as judged from the fold-induction of NFkB-inducible genes). As expected however, mRNAs corresponding to known inflammatory genes are significantly less abundant in response to the non-invasive SPI1/2 knockout strain, compared to wild-type infection. These data indicate, that endotoxin-tolerance renders macrophages largely insensitive to extracellular, but not to intracellular bacteria. ***This submission represents the mRNA component of the study
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Project description:DNA microarrays were used to provide a global transcriptional profile of S. typhimurium during the intracellular growth phase of infection pathogenesis following infection of macrophages.
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