Faecalibaculum rodentium strain:Alo17
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ABSTRACT:
PROVIDER: PRJNA282363 | ENA |
REPOSITORIES: ENA
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Project description:to investigate global gene expression of C. rodentium strain ICC169 and its isogenic pstCA and phoB mutants when grown in phosphate-rich and phosphate-low medium Genotype: 3 levels (wt, pstCA, phoB) phosphate: 2 levels (low, high)
2012-12-25 | E-GEOD-40906 | biostudies-arrayexpress
Project description:<p>The global rise in maternal obesity increases the risk of adverse maternal and neonatal outcomes. This study demonstrates that both long- (12 weeks) and short-term (gestational) exposure to a high-fat diet (HFD) induces uterine labor disorders, elevates stillbirth rates, and alters gut microbiota composition. Fecal microbiota transplantation (FMT) reveals that HFD inhibits uterine AMPK phosphorylation and reduces COX4 expression via gut microbiota modulation, further contributing to labor dysfunction. Faecalibaculum rodentium, a dominant gut bacterium, shows a negative correlation with stillbirth incidence. Transplantation of Faecalibaculum rodentium mitigates HFD-induced labor disorders, restores uterine ATP levels, and reduces stillbirth rates. This intervention increases serum butyric and acetic acid levels, which inhibit ERK phosphorylation via the GPR41 receptor and activate AMPK phosphorylation, promoting Nrf1 and PGC1 expression. These findings highlight the pivotal role of Faecalibaculum rodentium in counteracting HFD-induced uterine mitochondrial dysfunction and stillbirth.</p>
2025-08-22 | MTBLS12877 | MetaboLights
Project description:Citrobacter rodentium strain:DBS100 Genome sequencing
| PRJNA527323 | ENA
Project description:to investigate global gene expression of C. rodentium strain ICC169 and its isogenic pstCA and phoB mutants when grown in phosphate-rich and phosphate-low medium
2012-12-25 | GSE40906 | GEO
Project description:Citrobacter rodentium is a murine pathogen used to model the intestinal infection caused by Enteropathogenic and Enterohemorrhagic Escherichia coli (EPEC and EHEC), two diarrheal pathogens responsible for morbidity and mortality in developing and developed countries, respectively. During infection, these bacteria must sense and adapt to the gut environment of the host. In order to adapt to changing environmental cues and modulate expression of specific genes, bacteria can use two-component signal transduction systems (TCS). We have shown that the deletion of the Cpx TCS in C. rodentium leads to a marked attenuation in virulence in C3H/HeJ mice. In E. coli, the Cpx TCS is reportedly activated in response to signals from the outer-membrane lipoprotein NlpE. We therefore investigated the role of NlpE in C. rodentium virulence. We also assessed the role of the reported negative regulator of CpxRA, CpxP. We found that as opposed to the ΔcpxRA strain, neither the ΔnlpE, ΔcpxP nor the ΔnlpE/ΔcpxP strains were significantly attenuated, and had similar in vivo localization to wild-type C. rodentium. The in vitro adherence of the Cpx auxiliary protein mutants, ΔnlpE, ΔcpxP, ΔnlpEΔcpxP, was comparable to wild-type C. rodentium, whereas the ΔcpxRA strain showed significantly decreased adherence. To further elucidate the mechanisms behind the contrasting virulence phenotypes, we performed microarrays in order to define the regulon of the Cpx TCS. We detected 393 genes differentially regulated in the ΔcpxRA strain. The gene expression profile of the ΔnlpE strain is strikingly different than the profile of ΔcpxRA with regards to the genes activated by CpxRA. Further, there is no clear inverse correlation in the expression pattern of the ΔcpxP strain in comparison to ΔcpxRA. Interestingly, 161 genes were downregulated in the ΔcpxRA strain while being upregulated or unchanged in all other Cpx auxiliary protein deletion strains. This group of genes include T6SS, ompF and the regulator for colanic acid synthesis, that may contribute to the loss of virulence of ΔcpxRA. Taken together, these data suggest that in these conditions, CpxRA activates gene expression in a largely NlpE- and CpxP-independent manner.
2018-12-26 | GSE114699 | GEO
Project description:Citrobacter rodentium Genome sequencing
| PRJNA261533 | ENA
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:The identification of Atg16L1 as a susceptibility gene has implicated antibacterial autophagy in the pathogenesis of Crohn's disease, a major type of inflammatory bowel disease (IBD). However, the role of Atg16L1 during extracellular bacterial infections of the intestine has not been sufficiently examined and compared to the function of other IBD susceptibility genes such as Nod2. We now find that Atg16L1 mutant mice are extraordinarily resistant to intestinal disease induced by the model bacterial pathogen Citrobacter rodentium. We further demonstrate that Atg16L1 deficiency alters the intestinal environment to mediate an enhanced immune response that is dependent on monocytic cells, and that Atg16L1/Nod2 double mutant mice lose this advantage. These results reveal an unappreciated immuno-suppressive function of an IBD gene, and raise the possibility that gene variants that affect the autophagy pathway were evolutionarily maintained to protect against certain life-threatening infections. Twenty samples have been analyzed. All are colonic tissue from mice. Controls are uninfected WT mice, uninfected Atg16L1 mutant mice (Atg16L1HM) (n=3/genotype). Treatment conditions are tissue from WT and Atg16L1 mutant mice 6 days after C. rodentium infection (n=4/genotype) and 15 days after infection (n=3/genotype).
2013-11-27 | E-GEOD-49109 | biostudies-arrayexpress