Citrobacter rodentium
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA111057 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Previous experiments have shown that hexuronates regulate EHEC virulence, here we look at glucuronic acid effect on citrobacter rodentium
2024-01-09 | GSE252543 | GEO
Project description:Previous experiments have shown that hexuronates regulate EHEC virulence, here we look at glucuronic acid effect on citrobacter rodentium
2024-01-13 | GSE252823 | GEO
Project description:Identification of the targets of RegA with and without bicarbonate stimulation by comparing RegA knockout to multicopy RegA transgenics. RegA is an AraC like transcription factor identified in a mutational screen for virulence genes in Citrobacter rodentium, an attaching and effacing pathogen that causes transmissible colonic hyperplasia in mice. This experiment compares the RegA null strain with a multicopy plasmid rescue of this null strain in the presence and absence of bicarbonate with the aim of identifying pathogenesis related genes related to the early and late stages of attachment and effacement. Keywords: genetic modification, transcription factor, induction A strain of Citrobacter rodentium with a knockout of RegA was compared to the same strain rescued with a multicopy plasmid containing the wildtype RegA gene. These strains were analyzed with and without bicarbonate in an unconnected two factor design with dye balanced biological replicates.
2010-05-19 | E-GEOD-12876 | biostudies-arrayexpress
Project description:Transcriptome analysis of infected and uninfected mice with Citrobacter rodentium
2018-09-21 | GSE111097 | GEO
Project description:Identification of the targets of RegA with and without bicarbonate stimulation by comparing RegA knockout to multicopy RegA transgenics. RegA is an AraC like transcription factor identified in a mutational screen for virulence genes in Citrobacter rodentium, an attaching and effacing pathogen that causes transmissible colonic hyperplasia in mice. This experiment compares the RegA null strain with a multicopy plasmid rescue of this null strain in the presence and absence of bicarbonate with the aim of identifying pathogenesis related genes related to the early and late stages of attachment and effacement. Keywords: genetic modification, transcription factor, induction
2008-09-22 | GSE12876 | GEO
Project description:To determine the role of the liver in coordinating systemic immune responses to enteric infection, matched measurements of global gene expression profiles were collected from the murine liver and intestinal epithelium throughout the course of enteric infection and clearance of Citrobacter rodentium, a mouse model of infectious colitis
2026-07-29 | GSE326680 | GEO
Project description:Opioids analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit their use. It has been recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. Further study indicated distinct alterations in the gut microbiome and metabolome following morphine treatment, contributing to the negative consequences associated with opioid use. However, it is unclear how opioids modulate gut homeostasis in the context of a hospital acquired bacterial infection. In the current study, a mouse model of C. rodentium infection was used to investigate the role of morphine in the modulation of gut homeostasis in the context of a hospital acquired bacterial infection. Citrobacter rodentium is a natural mouse pathogen that models intestinal infection by enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) and causes attaching and effacing lesions and colonic hyperplasia. Morphine treatment resulted in 1) the promotion of C. rodentium systemic dissemination, 2) increase in virulence factors expression with C. rodentium colonization in intestinal contents, 3) altered gut microbiome, 4) damaged integrity of gut epithelial barrier function, 5) inhibition of C. rodentium-induced increase in goblet cells, and 6) dysregulated IL-17A immune response. This is the first study to demonstrate that morphine promotes pathogen dissemination in the context of intestinal C. rodentium infection, indicating morphine modulates virulence factor-mediated adhesion of pathogenic bacteria and induces disruption of mucosal host defense during C. rodentium intestinal infection in mice. This study demonstrates and further validates a positive correlation between opioid drug use/abuse and increased risk of infections, suggesting over-prescription of opioids may increase the risk in the emergence of pathogenic strains and should be used cautiously. Therapeutics directed at maintaining gut homeostasis during opioid use may reduce the comorbidities associated with opioid use for pain management.
2020-02-18 | E-MTAB-7503 | biostudies-arrayexpress
Project description:ChIP-seq of H-NSchr, HppXCROD2, and sigma 70 in Citrobacter rodentium ICC168 and E. coli MG1655
2026-05-25 | E-MTAB-17049 | biostudies-arrayexpress
Project description:SILAC experiment to investigate proteome changes in response to the disruption of CPX in Citrobacter rodentium ICC168.
2019-01-07 | PXD009049 | Pride
Project description:This dataset comprises a non-targeted metabolomics study of a Citrobacter rodentium-induced colitis mouse model, analyzed using high-resolution mass spectrometry in electrospray ionization (ESI) negative mode. The study employs reversed-phase liquid chromatography (RPLC) to profile metabolic alterations associated with infection-induced inflammation.
2025-03-21 | MSV000097399 | MassIVE