Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1295396 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The intestines house a diverse microbiota that must compete for nutrients to survive, but the specific limiting nutrients that control pathogen colonization are not clearly defined. Clostridioides difficile colonization typically requires prior disruption of the microbiota, suggesting that outcompeting commensals for resources is key in establishing C. difficile infection (CDI). The immune protein calprotectin (CP) is released into the gut lumen during CDI to chelate zinc (Zn) and other essential nutrient metals. Yet, the impact of Zn limitation on C. difficile colonization is unknown. To define C. difficile responses to Zn limitation, we performed RNA sequencing on C. difficile exposed to CP. In media with CP, C. difficile upregulated genes involved in metal homeostasis and amino acid metabolism.
2019-10-24 | GSE135912 | GEO
Project description:Gene expression level of Clostridioides difficile (C. difficile) strain R20291 comparing control C. difficile carring pMTL84151 as vector plasmid with C. difficile conjugated with a pMTL84151-03890 gene. Goal was to determine the effects of 03890 gene conjugation on C. difficile strain R20291 gene expression.
2023-11-30 | GSE219066 | GEO
Project description:Detection of clostridithiols from heterologous expression of one or both putative genes for clostridithiol biosynthesis (originating from Clostridioides difficile wild-type 630) in liquid cultures of E. coli BL21(DE3) grown in modified minimal medium
2025-06-12 | MSV000098169 | MassIVE
Project description:High-fat diet rewires gut host-microbiota relationship to derive worse outcomes following Clostridioides difficile infection
2026-02-16 | GSE313697 | GEO
Project description:Clostridioides difficile interactions with the gut mucosa are crucial for colonisation and establishment of infection, however key infection events during the establishment of disease are still poorly defined. To better understand the initial events that occur during C. difficile colonisation, we employed a dual RNA-sequencing approach to study the host and bacterial transcriptomic profiles during C. difficile infection in a dual-environment in vitro human gut model. Temporal changes in gene expression were analysed over 3-24h post infection and comparisons were made with uninfected controls.
2023-03-23 | E-MTAB-12660 | biostudies-arrayexpress
Project description:To reveal the effects of deleting the Δxtr gene in Clostridioides difficile, we first constructed a Δxtr knockout mutant and then examined the resulting phenotypic changes. Finally, to elucidate the underlying mechanisms, we performed RNA-sequencing-based transcriptome analysis.
2025-12-30 | E-MTAB-15575 | biostudies-arrayexpress
Project description:Clostridioides difficile can cause severe infections in the gastrointestinal tract and affects almost half a million people in the U.S every year. Upon establishment of infection, a strong immune response is induced. We sought to investigate the dynamics of the mucosal host response during C. difficile infection.
2023-09-13 | GSE237574 | GEO
Project description:Clostridioides difficile infection (CDI), caused by strains producing toxin B (TcdB), poses a significant global health threat. While C. difficile exhibits substantial diversity, functional studies have focused on a limited number of isolates, overlooking other genomospecies within the genus. We describe five isolates from patients suspected of having CDI who tested negative for the PaLoc marker gene tcdC. Through genomic, proteomic, and phenotypic analyses, we demonstrate that they correspond to three novel toxin-producing species, designated as Clostridioides cryptodifficilis sp. nov., Clostridioides divergens sp. nov., and Clostridioides subdifficilis sp. nov. These species are distinguished by unique MALDI-ToF signatures, metabolic capabilities, and genomic and proteomic architectures, underscoring their clear taxonomic and functional divergence from C. difficile. They secrete functionally active TcdB7 or TcdB11, as demonstrated by cytotoxicity assays in cultured cells and in vivo using the mouse ileal loop model, implicating them in disease pathology, albeit with lower virulence than C. difficile. Our findings expand the known diversity of TcdB-producing Clostridioides and have direct implications for diagnostics, surveillance, and clinical management of diarrheal diseases.
2026-05-06 | PXD067952 | Pride
Project description:Clostridioides difficile infection (CDI), caused by strains producing toxin B (TcdB), poses a significant global health threat. While C. difficile exhibits substantial diversity, functional studies have focused on a limited number of isolates, overlooking other genomospecies within the genus. We describe five isolates from patients suspected of having CDI who tested negative for the PaLoc marker gene tcdC. Through genomic, proteomic, and phenotypic analyses, we demonstrate that they correspond to three novel toxin-producing species, designated as Clostridioides cryptodifficilis sp. nov., Clostridioides divergens sp. nov., and Clostridioides subdifficilis sp. nov. These species are distinguished by unique MALDI-ToF signatures, metabolic capabilities, and genomic and proteomic architectures, underscoring their clear taxonomic and functional divergence from C. difficile. They secrete functionally active TcdB7 or TcdB11, as demonstrated by cytotoxicity assays in cultured cells and in vivo using the mouse ileal loop model, implicating them in disease pathology, albeit with lower virulence than C. difficile. Our findings expand the known diversity of TcdB-producing Clostridioides and have direct implications for diagnostics, surveillance, and clinical management of diarrheal diseases.
2026-05-06 | PXD066931 | Pride
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