Macrophages infected with Salmonella
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE503 | GEO | 2003/07/16
SECONDARY ACCESSION(S): PRJNA85217
REPOSITORIES: GEO
Similar Datasets
Project description:Infection with Salmonella enterica serovar Typhi in humans causes the systemic, life-threatening disease typhoid fever. In the laboratory, typhoid fever can be modeled through the inoculation of susceptible mice with Salmonella enterica serovar Typhimurium. The ensuing disease is characterized by systemic dissemination and colonization of many organs, including the liver, spleen and gallbladder. Using this murine model, we previously characterized the interactions between Salmonella Typhimurium and host cells in the gallbladder and showed that this pathogen can successfully invade gallbladder epithelial cells and proliferate. Additionally, we showed that Salmonella Typhimurium can use bile phospholipids to grow at high rates. These abilities are likely important for quick colonization of the gallbladder during typhoid fever and further pathogen dissemination through fecal shedding. To further characterize the interactions between Salmonella and the gallbladder environment we compared the transcriptome of Salmonella cultures grown in LB or physiological murine bile. Our data showed that many genes involved in bacterial central metabolism are affected by bile, with the citric acid cycle being repressed and alternative respiratory systems being activated. Additionally, our study revealed a new aspect of Salmonella interactions with bile through the identification of phoP as a bile-responsive gene. Repression of phoP expression does not involve PhoPQ sensing of a bile component. Due to its critical role in Salmonella virulence, further studies in this area will likely reveal aspects of the interaction between Salmonella and bile that are relevant to disease.
2011-11-10 | GSE33604 | GEO
Project description:In many Gram-negative bacteria, the stress sigma factor of RNA polymerase, σS/RpoS, remodels global gene expression to reshape the physiology of quiescent cells and ensure their survival under non-optimal growth conditions. In the foodborne pathogen Salmonella enterica serovar Typhimurium, σS is also required for biofilm formation and virulence. We have recently shown that a ΔrpoS mutation affects the magnesium content of Salmonella and expression of the primary Mg2+-transporter CorA. The other two Mg2+-transporters of Salmonella are encoded by the PhoP-activated mgtA and mgtB genes expressed under magnesium starvation, whereas the corA gene is expressed constitutively. The σS control of corA prompted us to evaluate the impact CorA in quiescent Salmonella cells, by using global and analytical proteomic analyses and physiological assays. The ΔcorA mutation conferred a competitive disadvantage to exit from stationary phase, and slightly impaired motility, but had no effect on total and free cellular magnesium contents. In contrast to the wild type strain, the ΔcorA mutant produced MgtA, but not MgtB, in the presence of high extracellular magnesium concentration. Under these conditions, MgtA production in the ΔcorA mutant did not require PhoP and, consistently, a ΔmgtA, but not a ΔphoP, mutation slightly reduced the magnesium content of the ΔcorA mutant. Nevertheless, the ΔphoP mutation strongly impaired growth and motility, in the absence of CorA only and independently of the extracellular magnesium concentration, unraveling the importance of PhoP-dependent functions in the absence of CorA. Under these conditions, several proteins involved in flagella formation, chemotaxis and secretion were affected by the ΔcorA and ΔphoP mutations in combination, but not alone. Altogether, our data pinpoint a regulatory network, where the absence of CorA is sensed and its physiological consequences alleviated by induction of MgtA- and PhoP- dependent compensatory mechanisms.
2023-10-24 | PXD041489 | Pride
Project description:Bacteria possess many small noncoding RNAs whose regulatory roles in pathogenesis are little understood due to a paucity of macroscopic phenotypes in standard virulence assays. Here, we use a novel Dual RNA-seq approach for a single-step simultaneous RNA profiling in both pathogen and host to reveal molecular phenotypes of sRNAs during infection with Salmonella Typhimurium. We identify a new PhoP/Q-activated small RNA which upon bacterial internalization acts to temporally control the expression of both, invasion-associated effectors and virulence genes required for intracellular survival. This riboregulatory activity is shown to adjust the human response to replicating Salmonella, and have a pervasive impact on host RNA expression both inside and outside protein-coding regions including infection-specific alterations of an array of long noncoding RNAs. Our study provides a paradigm for a comprehensive RNA-based analysis of intracellular bacterial pathogens without their physical purification from a host and a new discovery route for hidden functions of pathogen genes.
2015-12-11 | GSE67948 | GEO
Project description:Global expression profiles of Salmonella typhi grown in the supernatant of infection and within human macrophages at 0h, 2h, 8h and 24h were obtained. Stringent analytical methods were used to compare Salmonella typhi cDNAs and revealed that known virulence factors, such as the SPI-1 and SPI-2 encoded type III secretion systems, were found to be expressed as predicted during infection by Salmonella. Intracellular Typhi expressed many genes encoding antimicrobial peptides, used the glyoxylate bypass for fatty acid utilization, and, did not induce the SOS response or the oxidative stress response. Genes coding for the flagellar apparatus, chemotaxis and the iron transport system were down-regulated in vivo. The combined use of SCOTS and microarray is an effective way to determine global bacterial gene expression profiling in the context of host infection, without the need of increasing the multiplicity of infection beyond what is seen in nature. Keywords: Time course
2006-01-10 | GSE3096 | GEO
Project description:RNA from in vitro grown Salmonella typhimurium is compared with RNA extracted from Salmonella typhimurium from infected chick caecums using a common DNA reference. Keywords: Disease state analysis, infected versus uninfected, common reference
2008-02-12 | GSE10337 | GEO
Project description:Salmonella must express and deploy a type III secretion system located in Salmonella pathogenicity island 2 (SPI-2) in order to survive in host phagocytic vacuoles and to cause systemic infection in mouse models of typhoid fever. A genome-wide approach to screening for Salmonella genes that are transcriptionally co-regulated in vitro with SPI-2 genes was used to identify bacterial loci that might function in a mouse model of systemic disease. Strains with mutations in three SPI-2 co-expressed genes were constructed and tested for their ability to cause disease in mice. We found that virK, a homologue of a Shigella virulence determinant, and rcsC, a sensor kinase, are important at late stages of infection. A second Salmonella gene that has VirK homology, somA, is also important for systemic infection in mice. We have shown that expression of both virK and somA requires the transcription factor PhoP, whereas rcsC does not. Additionally, rcsC expression does not require the transcription factor OmpR, but expression of one of the known targets of RcsC, the yojN rcsB putative operon, does require OmpR. virK, somA and rcsC are expressed in tissue culture macrophages and confer Salmonella resistance to the cationic peptide polymyxin B. We conclude that virK, somA and rcsC are important for late stages of Salmonella enteric fever, and that they probably contribute to the remodelling of the bacterial outer membrane in response to the host environment.
2005-10-07 | E-SMDB-1981 | biostudies-arrayexpress
Project description:Poultry products are an important source of Salmonella enterica. An effective way to reduce food poisoning due to Salmonella would be to breed chickens more resistant to Salmonella. Unfortunately resistance to Salmonella is a complex trait with many factors involved. To learn more about Salmonella resistance mechanisms in young chickens, a cDNA microarray analysis was performed to compare gene expression profiles between a Salmonella susceptible and a more resistant chicken line. Newly hatched chickens were orally infected with S. enterica serovar Enteritidis. Since the intestine is the first barrier the bacteria encountersbacteria encounter after oral inoculation, gene expression was investigated in the intestine, from day 1 until day 21 post infection. Differences in gene expression between the susceptible and resistant chicken line were found in control as well as Salmonella infected conditions. In response to the Salmonella infection, the expression of different sets of genes seemed to be affected in the jejunum of the two chicken lines. In the susceptible line this included genes that affect T-cell activation, whereas in the more resistant line, at day 1, macrophage activation seemed to be more affected. At day 7 and 9 most gene expression differences between the two chicken lines were identified under control conditions, indicating a difference in the intestinal development between the two chicken lines which might be linked to the difference in Salmonella susceptibility. The findings in this study have lead to the identification of novel genes and possible cellular pathways of the host involved in Salmonella susceptibility. Keywords: timecourse, disease
2005-12-05 | GSE3066 | GEO
Project description:FinO-domain proteins such as ProQ of the model pathogen Salmonella enterica have emerged as a new class of major RNA-binding proteins in bacteria. ProQ has been shown to target hundreds of transcripts including mRNAs from many virulence regions but its role, if any, in bacterial pathogenesis has not been studied. Here, using a Dual RNA-seq approach to profile ProQ-dependent gene expression changes as Salmonella infects human cells, we reveal dysregulation of bacterial motility, chemotaxis and virulence genes which is accompanied by altered mitogen-activated protein kinase signaling in the host. Comparison with Hfq, Salmonella’s other major RNA chaperone, reinforces the notion that these two global RNA binding proteins work in parallel to ensure full virulence. Of newly discovered infection-associated ProQ-bound small noncoding RNAs, we show that STnc540 represses a virulence-related magnesium transporter mRNA in a ProQ-dependent manner. Together, this comprehensive study uncovers the relevance of ProQ for Salmonella infection and highlights the importance of RNA-binding proteins in regulating bacterial virulence programs.
2018-11-28 | GSE117255 | GEO
Project description:FinO-domain proteins such as ProQ of the model pathogen Salmonella enterica have emerged as a new class of major RNA-binding proteins in bacteria. ProQ has been shown to target hundreds of transcripts including mRNAs from many virulence regions but its role, if any, in bacterial pathogenesis has not been studied. Here, using a Dual RNA-seq approach to profile ProQ-dependent gene expression changes as Salmonella infects human cells, we reveal dysregulation of bacterial motility, chemotaxis and virulence genes which is accompanied by altered mitogen-activated protein kinase signaling in the host. Comparison with Hfq, Salmonella’s other major RNA chaperone, reinforces the notion that these two global RNA binding proteins work in parallel to ensure full virulence. Of newly discovered infection-associated ProQ-bound small noncoding RNAs, we show that STnc540 represses a virulence-related magnesium transporter mRNA in a ProQ-dependent manner. Together, this comprehensive study uncovers the relevance of ProQ for Salmonella infection and highlights the importance of RNA-binding proteins in regulating bacterial virulence programs.
2018-11-28 | GSE117252 | GEO
Project description:As the leading cause of food-borne illness in the world, Salmonella have evolved a sophisticated machinery to alter host cell function to promote virulence and survival.In this study, we compare production of non-coding RNAs between Salmonella-infected cells and mock infection cells. Using Solexa deep sequencing, we detected a panel of 19-24nt Salmonella-derived non-coding RNA fragments with considerable large copy numbers in human colonic epithelial HT-29 cells following Salmonella infection.The fragment with the highest copy number, Sal-1, was further validated by both quantitative reverse transcription polymerase chain reaction (qRT-PCR) and northern blot. The generation of Sal-1 requires the infection of host cells by Salmonella, and the processing of the Sal-1 M-bM-^@M-^\primaryM-bM-^@M-^] or M-bM-^@M-^\precursorM-bM-^@M-^] to the mature Sal-1 in Salmonella-infected cells is Dicer-independent but Argonaute 2 (Ago2)-dependent. Functionally, Sal-1 suppresses the expression of colonic epithelial cell endogenous inducible nitric oxide synthase (iNOS) via targeting its open reading frame and thus reduces the bacterial resistance of host cells. Screening and identification of Salmonella-encoded microRNA-like RNA fragments
2014-12-23 | E-GEOD-53586 | biostudies-arrayexpress