Clostridioides difficile
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ABSTRACT:
PROVIDER: PRJNA128571 | ENA |
REPOSITORIES: ENA
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Project description:Comparison of Clostridium difficile transcriptome of strain CD630E grown for 10 hours in PY (supplemented with mild concentration of cysteine) versus PYC (PY supplemented with 10 mM of cysteine). Experimental procedure was designed to investigate the influence of cysteine on toxins production and the regulatory network involved.
2013-12-31 | GSE22423 | GEO
Project description:Comparison of Clostridium difficile transcriptome of strain CD630E grown for 10 hours in PY (supplemented with mild concentration of cysteine) versus PYC (PY supplemented with 10 mM of cysteine). Experimental procedure was designed to investigate the influence of cysteine on toxins production and the regulatory network involved. two-conditions experiments, excess of cysteine vs mild concentration of cysteine, 4 biological replicates for each condition Description of the supplementary files: Main - Short description of the experiment Result_all - All significative genes Result_Gold* - High quality significative gene Result_Silver** - Medium quality significative gene All_Raw_data - All genes results significative and non significative Design_Genes-OUT - Genes not present in the platform Design_Genes-Oligos - Number of oligos design per gene * Gold : Nbr significative oligos = Nbr oligos designed for this gene ** Silver : Nbr significative oligos = Nbr oligos designed for this gene -1
2013-12-31 | E-GEOD-22423 | biostudies-arrayexpress
Project description:Clostridium difficile C630E: growth in TY with 30 mM proline vs. growth in TY alone
| PRJNA183177 | 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:Clostridioides difficile is the leading cause of nosocomial diarrhea, afflicting approximately half a million people each year in the USA, burdening both individuals’ quality of life and the healthcare system. In the gastrointestinal (GI) tract, C. difficile must acquire essential nutrients to colonize, establish infection, and persists in a polymicrobial environment. C. difficile is a cysteine auxotroph and the GI tract contains low levels of cysteine, highlighting gaps in our understanding of how C. difficile acquires this amino acid during infection. One possible source of cysteine for C. difficile during infection is glutathione (GSH), tripeptide thiol in mammalian cells. Our data indicate that C. difficile encodes two redundant enzymes (GecA and GecB) that allow it to use GSH as a source of cysteine. Using murine models of C. difficile infection, we also show that C. difficile uses its toxins to increase available GSH in the GI tract during infection. Finally, we show that the ability to utilize GSH gives wild-type C. difficile a fitness advantage over a GSH-deficient mutant in vivo. These findings establish GSH metabolism as a novel strategy of nutrient acquisition that links C. difficile metabolism and virulence and highlight GSH metabolism as possibly impactful target for future therapeutic development.
2026-06-10 | GSE310543 | GEO
Project description:The incidence of Clostridium difficile infection has been steadily rising over the past decade. Its increased rate is associated with the specific NAP1/BI/027 strains which are “hypervirulent” and have led to several large outbreaks since their emergence. However, the relation between their outbreaks and virulence regulation mechanisms remains unclear. It has been reported that the major virulence factor TcdA and TcdB in C. difficile could be repressed by cysteine. Here, we investigated functional and virulence-associated regulation of C. difficile R20291 in response to cysteine stress by using a time-resolved genome-wide transcriptional analysis. Dramatic changes of gene expression in C. difficile were revealed in functional categories related to transport, metabolism, and regulators under cysteine stress during different phases of growth.
2020-12-12 | GSE107961 | GEO
Project description:Clostridium difficile CD630E JIR8094: growth 10h with 0.5% glucose in TY vs growth 10h in TY
| PRJNA156173 | ENA
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:Clostridium difficile mutant ccpA CD630E JIR8094: growth 10h with 0.5% glucose in TY vs growth 10h in TY
| PRJNA156175 | ENA