S. Typhi ESBL
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Similar Datasets
Project description:Salmonella enterica serovar Typhi (S. Typhi), a human-restricted pathogen, enters the host through the gut to cause typhoid fever. Recent calculations of the typhoid fever burden estimated that more than 20 million new typhoid fever cases occur in low and middle-income countries, resulting in 129,000-223,000 deaths yearly. Interestingly, upon the resolution of acute disease, 1%-5% of patients become asymptomatic chronic carriers of S. Typhi. Chronically infected hosts are not only critical reservoirs of infection that transmit the disease to naive individuals but are also predisposed to developing gallbladder carcinoma (GBC). Nevertheless, the molecular mechanisms involved in the early interactions between gallbladder epithelial cells and S. Typhi remain largely unknown. Based on our previous studies showing that very closely related S. Typhi strains elicit distinct innate immune responses, we hypothesized that host molecular pathways activated by S. Typhi strains derived from acutely and chronically infected patients will differ. To test this hypothesis, we used a novel human organoid-derived polarized gallbladder monolayer (HODGM) model, and 13 S. Typhi strains derived from acutely (n=6) and chronically (n=7) infected patients. We found that S. Typhi strains derived from acutely and chronically infected patients differentially regulate mitogen-activated protein kinase (MAPK) and S6 transcription factors. This differential regulation impacts, at least in part, the cytokine signaling pathway involved in the production of TNF- and IL-6 and is likely to play a critical role in inducing chronic S. Typhi infection in the gallbladder.
2024-04-05 | GSE253700 | GEO
Project description:This study describes how Salmonella Typhi, the pathogen responsible for typhoid fever, uses similar strategies to escape immune defense responses and survive within its human host. To elucidate the early mechanisms of typhoid fever, we performed studies using healthy human intestinal tissue samples to analyze gene expression changes in human intestinal specimens and bacterial cells both separately and after colonization. Our results showed mechanistic strategies that S. Typhi uses to rearrange the cellular machinery of the host cytoskeleton to successfully invade the intestinal epithelium, promote polarized cytokine release and evade immune system activation by downregulating genes involved in antigen sampling and presentation during infection.
2018-06-15 | GSE113333 | GEO
Project description:Sequencing of RNA of selected Salmonella Typhi strains from typhoid-endemic regions of Asia and Africahttp://www.sanger.ac.uk/resources/downloads/bacteria/salmonella.htmlThese data are part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2015-01-20 | E-ERAD-315 | biostudies-arrayexpress
Project description:Human genetic diversity can reveal critical factors in host-pathogen interactions. This is especially useful for human-restricted pathogens like Salmonella enterica serovar Typhi (S. Typhi), the cause of Typhoid fever. One key dynamic during infection is competition for nutrients: host cells attempt to restrict intracellular replication by depriving bacteria of key nutrients or delivering toxic metabolites in a process called nutritional immunity. Here, a cellular genome-wide association study of intracellular replication by S. Typhi in nearly a thousand cell lines from around the world—and extensive follow-up using intracellular S. Typhi transcriptomics and manipulation of magnesium concentrations—demonstrates that the divalent cation channel mucolipin-2 (MCOLN2) restricts S. Typhi intracellular replication through magnesium deprivation. Our results reveal natural diversity in Mg2+ limitation as a key component of nutritional immunity against S. Typhi.
2023-01-05 | GSE222194 | GEO
Project description:In this study participants were experimentally challenged with an infective dose of S. Typhi (1-5x10^3-4 cfu) and followed over at least 14 days. Every study participant was treated with antibiotics (ciprofloxacin, 500 mg twice daily, 14 days) on day 14 after challenge unless diagnosed with typhoid fever at which time treatment commenced immediately (ciprofloxacin, 500 mg twice daily, 14 days). For details about the study design please refer to Waddington et al. CID 2014 May;58(9):1230-40. Criteria for typhoid diagnosis were either microbiological (≥1 positive blood culture collected after day 5) and/or clinical (fever ≥38°C sustained for ≥12hrs). 3mL of venous blood was obtained at pre-challenge baselines, 24hrs prior typhoid diagnosis, day of diagnosis, 24hrs post-diagnosis and day 14 after challenge in those diagnosed with acute typhoid fever. In those who did not develop typhoid despite oral challenge samples were obtained at pre-challenge, day 7 and day 14 after challenge. The samples are labelled with one of the following accronyms: V1: Day 0, i.e. pre-challenge control. D7: day 7 after challenge. TD-24: 24hrs prior to typhoid diagnosis. TD: day of typhoid diagnosis. TD+24: 24hrs after typhoid diagnosis. D14: day 14 after challenge.
2015-10-01 | E-MTAB-3423 | biostudies-arrayexpress
Project description:Six sequencing libraries was prepared from S. Typhi planktonic cells and biofilm cells using Illumina HiSeq 2500 sequencing to investigate differential gene expression between the two conditions. The transcriptome was processed using Cufflinks and there were a total of 35 up-regulated genes and 29 down-regulated genes log2-fold change values of greater than 2 and less than negative 2. The differentially expressed genes were identified using BLAST and the functions was analysed. This study provides an overview of the genes that are differentially expressed in S. Typhi when it transitions from the planktonic to the biofilm phenotype. The data will provide a basis for further study is necessary to uncover the mechanisms of biofilm formation in S. Typhi and discovery of novel gene functions or pathways associated with the development of the typhoid carrier state. This data may also be used to elucidate the effect of biofilm on the virulence and pathogenicity of S. Typhi in chronic carriers.
2017-10-31 | GSE93686 | GEO
Project description:Bacterial pathogens causing systemic disease commonly evolve from organisms associated with localized infections but differ from their close relatives in their ability to overcome mucosal barriers by mechanisms that remain incompletely understood. Here we investigated whether acquisition of a regulatory gene, tviA, contributed to the ability of Salmonella enterica serotype Typhi to disseminate from the intestine to systemic sites of infection during typhoid fever. To study the consequences of acquiring a new regulator by horizontal gene transfer, tviA was introduced into the chromosome of S. enterica serotype Typhimurium, a closely related pathogen causing a localized gastrointestinal infection in immunocompetent individuals. Modulation of gene expression by TviA in serotype Typhi and Typhimurium was determined by profiling and found to be very comparable. Expression of flagellin, a pathogen associated molecular pattern (PAMP), was repressed by TviA when bacteria were grown at osmotic conditions encountered in tissue, but not at higher osmolarity present in the intestinal lumen. TviA-mediated flagellin repression enabled bacteria to evade sentinel functions of human model epithelia and resulted in increased bacterial dissemination to the spleen in a chicken model.
2010-07-07 | GSE20321 | GEO
Project description:Typhoid fever is caused by the Gram-negative bacterium Salmonella enterica serovar Typhi. Bulk RNA-sequencing (RNA-seq) data were generated from blood samples obtained from adult human volunteers enrolled in a vaccine trial involving two vaccines against typhoid fever, a plain polysaccharide vaccine, ViPS and a glycoconjugate vaccine, ViTCV. The participants were then challenged with S. Typhi in a controlled human infection model (CHIM).
2023-07-19 | GSE217667 | GEO
Project description:In this study, whole blood samples were used to determine the gene expression of healthy adult volunteers experimentally challenged with S. Typhi Quailes strain. Samples were collected at baseline (pre-challenge; Group: CTRL) and 7 days after challenge (Group: sEF) in individuals who did not reach diagnostic criteria. In those reaching the diagnostic endpoint (typhoid fever; Group: EF) the sample on the day of diagnosis when antibiotic treatment commenced was taken. These samples were derived from the placebo arm of a recent a Single Centre, Randomised, Doubleblind, Placebo Controlled Study to Evaluate M01ZH09 in a Healthy Adult Challenge Model, Using Ty21a Vaccine as a Positive Control. Darton et al. PMID: 27533046.
2019-09-02 | GSE112958 | GEO
Project description:Salmonella enterica serovar Typhi producing CTX-M-15 extended spectrum β-lactamase in the Democratic Republic of the Congo
| PRJEB19771 | ENA