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ABSTRACT: FMT in recurrent C. Difficile and or IBD (inflammatory bowel diseases)

PROVIDER: PRJNA744877 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15070300.fastq.gz	Fastqsanger.gz
	SRR15070301.fastq.gz	Fastqsanger.gz
	SRR15070302.fastq.gz	Fastqsanger.gz
	SRR15070303.fastq.gz	Fastqsanger.gz
	SRR15070304.fastq.gz	Fastqsanger.gz

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Project description:FMT in recurrent C. Difficile and or IBD (inflammatory bowel diseases)

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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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Common functional alterations identified in blood transcriptome of autoimmune cholestatic liver and inflammatory bowel diseases

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