Clostridioides difficile
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ABSTRACT:
PROVIDER: PRJNA183177 | ENA |
REPOSITORIES: ENA
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Project description:Clostridium difficile, a proteolytic Gram-positive anaerobe, has emerged as a significant nosocomial pathogen. Stickland fermentation reactions are thought to be important for growth of C. difficile. In Stickland reactions, pairs of amino acids donate and accept electrons, generating ATP and reducing power in the process. Reduction of the electron acceptors proline and glycine requires the D-proline reductase (PR) and the glycine reductase (GR) enzyme complexes, respectively. PrdR, a sigma54-dependent regulator, activates transcription of the PR-encoding genes in the presence of proline and negatively regulates the GR-encoding genes, suggesting that PrdR is a central metabolism regulator that controls preferential utilization of proline and glycine to produce energy via the Stickland reactions. Here, transcriptional profiling of C. difficile comparing growth in TY medium supplemented with 30 mM L-proline to growth in TY medium alone is performed.
2015-10-01 | GSE42469 | GEO
Project description:Clostridium difficile CD630E JIR8094: growth 10h with 0.5% glucose in TY vs growth 10h in TY
| PRJNA156173 | ENA
Project description:Clostridium difficile mutant ccpA CD630E JIR8094: growth 10h with 0.5% glucose in TY vs growth 10h in TY
| PRJNA156175 | ENA
Project description:We illustrate how metabolically distinct species of Clostridia can protect against or worsen Clostridioides difficile infection, modulating the pathogen's colonization, growth, and virulence to impact host survival. Gnotobiotic mice colonized with the amino acid fermenter Paraclostridium bifermentans survived infection while mice colonized with the butyrate-producer, Clostridium sardiniense, more rapidly succumbed. Systematic in vivo analyses revealed how each commensal altered the gut nutrient environment, modulating the pathogen's metabolism, regulatory networks, and toxin production. Oral administration of P. bifermentans rescued conventional mice from lethal C. difficile infection via mechanisms identified in specifically colonized mice. Our findings lay the foundation for mechanistically informed therapies to counter C. difficile disease using systems biologic approaches to define host-commensal-pathogen interactions in vivo.
2021-10-04 | GSE182613 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE35070: Comparison of the expression profiles of 630E JIR8094 strain and a ccpA mutant after 10h of growth in TY with 0.5% glucose. GSE35071: Comparison of the expression profiles of 630E JIR8094 strain and a ccpA mutant after 10h of growth in TY. GSE35072: Clostridium difficile CD630E JIR8094: growth 10h with 0.5% glucose in TY vs growth 10h in TY GSE35073: Clostridium difficile mutant ccpA CD630E JIR8094: growth 10h with 0.5% glucose in TY vs growth 10h in TY Refer to individual Series
2012-10-02 | E-GEOD-35152 | biostudies-arrayexpress
Project description:Clostridium difficile CD630E: growth with 10 mM cysteine in PY vs growth in PY
| PRJNA128571 | ENA
Project description:transcriptionnal profiling of a C. difficile strain JIR8094 comparing growth 10h in 0.5% TY medium with growth 10h in TY medium
2012-10-02 | GSE35072 | GEO
Project description:Clostridioides difficile is one of the most common nosocomial pathogens and a global public health threat. Upon colonization of the gastrointestinal tract, C. difficile is exposed to a rapidly changing polymicrobial environment and a dynamic metabolic milieu. Despite the link between the gut microbiota and susceptibility to C. difficile, the impact of synergistic interactions between the microbiota and pathogens on the outcome of infection is largely unknown. Here, we show that microbial cooperation between C. difficile and Enterococcus has a profound impact on the growth, metabolism, and pathogenesis of C. difficile.. Through a process of nutrient restriction and metabolite cross-feeding, E. faecalis shapes the metabolic environment in the gut to enhance C. difficile fitness and increase toxin production. These findings demonstrate that members of the microbiota, such as Enterococcus, have a previously unappreciated impact on C. difficile behavior and virulence.
2022-09-17 | GSE165751 | GEO
Project description:transcriptionnal profiling of a ccpA mutant of C. difficile strain JIR8094 comparing growth 10h in 0.5% TY medium with growth 10h in TY medium
2012-10-02 | GSE35073 | GEO
Project description:The response to iron limitation of several bacteria is regulated by the ferric uptake regulator (Fur). The Fur-regulated transcriptional, translational and metabolic networks of the Gram-positive, pathogen Clostridioides difficile were investigated by a combined RNA sequencing, proteomic, metabolomic and electron microscopy approach. At high iron conditions (760 g/l) the C. difficile fur mutant displayed a growth deficiency compared to wild type C. difficile cells. Several iron transporters were found induced by Fur regulation during low iron (11 g/l) conditions. The major adaptation to low iron conditions was observed for the central energy metabolism. Most ferredoxin-dependent amino acid fermentations were found significantly down regulated (had, etf, acd, grd, trx, bdc, hbd). The substrates of these pathways phenylalanine, leucine, glycine and some initial intermediates (phenylpyruvate, oxo-isocaproate, 3-hydroxy-butanoyl-CoA, crotonyl-CoA) were found accumulated, while some end product like isocaproate and butanoate were found reduced. Flavodoxin (fldX) formation and riboflavin biosynthesis (rib) were found enhanced, most likely to replace the missing ferredoxins. Proline reductase (prd), the corresponding ion pumping RNF complex (rnf) and the reaction product 5-aminovalerate were significantly enhanced. An ATP forming ATPase (atpCDGAHFEB,) of the F0F1-type was found induced while the formation of a V-type, mostly proton-pumping, ATP-consuming ATPase (atpDBAFCEKI, was decreased. The [Fe-S] enzyme-dependent pyruvate formate lyase (pfl), formate dehydrogenase (fdh) and hydrogenase (hyd) branch of glucose utilization and glycogen biosynthesis (glg) were significantly reduced, leading to an accumulation of glucose and pyruvate. The formation of [Fe-S] enzyme carbon monoxide dehydrogenase (coo) was inhibited. An intensive remodeling of the cell wall was observed most likely to increase antibiotic resistance. Polyamine biosynthesis (spe) was found induced leading to an accumulation of spermine, spermidine and putrescine. The fur mutant lost most of its flagella. Finally, the CRISPR/Cas and a prophage encoding operon were downregulated. Fur binding sites were found upstream of 20 of the regulated genes. Overall, adaptation to low iron conditions in C. difficile focused on an increase of iron import, significant decrease in metabolic iron utilization and protection during the complex transition.
2019-01-15 | GSE120189 | GEO