Non-toxigenic C. difficile
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB62683 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR11495271.fastq.gz | Fastqsanger.gz |
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Project description:Culture of toxigenic Clostridioides difficile
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Project description:Background: Clostridioides difficile (C. difficile) is a global threat and has significant implications for individuals and health care systems. Little is known about host molecular mechanisms and transcriptional changes in peripheral immune cells. This is the first gene expression study in whole blood of patients with C. difficile infection. Methods: We took blood and stool samples from patients with toxigenic C. difficile infection (CDI), non-toxigenic C. difficile infection (GDH), inflammatory bowel disease (IBD), diarrhoea from other causes (DC) and healthy controls (HC). We performed transcriptome-wide RNA profiling on peripheral blood to identify diarrhoea common and CDI unique gene sets. Results: Diarrhoea groups upregulated innate immune responses with neutrophils at the epicentre. The common signature associated with diarrhoea was non-specific and shared by various other inflammatory conditions. CDI had a unique 45-gene set reflecting downregulation of humoral and T cell memory functions. Dysregulation of immunometabolic genes was also abundant and linked to immune cell fate during differentiation. Conclusions: Whole transcriptome analysis of white cells in blood from patients with toxigenic C. difficile infection showed that there is an impairment of adaptive immunity and immunometabolism.
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Project description:The pathogenic bacterium Clostridioides difficile is a major cause of antibi-otic-associated diarrheal disease. Treatment of the disease is challenging because anti-biotics used for treatment may also perpetuate the conditions that contributed to initial susceptibility. Elucidating the mechanisms of C. difficile/intestinal epithelium interaction is needed to facilitate the development of new therapeutic options. The studies described in this communication demonstrate the development of a tissue culture system that supported the growth of C. difficile in co-culture with a model of the human intestinal epithelium produced from colonoids, organoids derived from human colonic biopsies. Epithelial cell responses to C. difficile included upregulation of CCL20, encoding a chemokine. Glucosylating toxin production by the bacteria was required for upregulation of CCL20. Additionally, bacteria associated with the monolayer in a non-toxin dependent manner. This system will support future investigation of epithelium/C. difficile interac-tions during CDI and identification of mechanisms that drive pathogenesis by C. difficile in the human intestine.
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