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Butyrate alters gene expression profiles in gBT-I cells

ABSTRACT: Butyrate alters gene expression profiles in gBT-I cells

PROVIDER: PRJNA547514 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9209731_1.fastq.gz	Fastqsanger.gz
	SRR9209731_2.fastq.gz	Fastqsanger.gz
	SRR9209732_1.fastq.gz	Fastqsanger.gz
	SRR9209732_2.fastq.gz	Fastqsanger.gz
	SRR9209733_1.fastq.gz	Fastqsanger.gz

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Butyrate alters gene expression profiles in gBT-I cells

Project description:Purpose: The aim of this study is to dissect if the microbiota-derived metabolite butyrate alters the transcriptome of antigen-activated CD8+ T cells. Methods: mRNA profiles from Ctrl and Butyrate-treated gBT-I were generated by deep sequencing, in triplicates, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: The analysis of RNAseq data of Ctrl and Butyrate-treated gBT-I lead to ~2,000 differentially expressed genes (FDR < 0.05; fold change>2). GSEA enrichment analysis revealed enrichment of memory T cells signatures in gBT-I following butyrate-treatment (Sarkar et al., 2008). Conclusions: Our data shows that butyrate alters the transcriptome of effector CD8+ T cells, in particular their memory signature.

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Exogenous butyrate inhibits butyrogenic metabolism and alters virulence phenotypes in Clostridioides difficile

Project description:The gut microbiome engenders colonization resistance against the diarrheal pathogen Clostridioides difficile but the molecular basis of this colonization resistance is incompletely understood. A prominent class of gut microbiome-produced metabolites important for colonization resistance against C. difficile is short chain fatty acids (SCFAs). In particular, one SCFA (butyrate) decreases the fitness of C. difficile in vitro and is correlated with C. difficile-inhospitable gut environments, both in mice and in humans. Here, we demonstrate that butyrate-dependent growth inhibition in C. difficile occurs under conditions where C. difficile also produces butyrate as a metabolic end product. Furthermore, we show that exogenous butyrate is internalized into C. difficile cells and is incorporated into intracellular CoA pools where it is metabolized in a reverse (energetically unfavorable) direction to crotonyl-CoA and (S)-3-hydroxybutyryl-CoA and/or 4-hydroxybutyryl-CoA. This internalization of butyrate and reverse metabolic flow of butyrogenic pathway(s) in C. difficile coincides with alterations in toxin release and sporulation. Together, this work highlights butyrate as a marker of a C. difficile inhospitable environment to which C. difficile responds by releasing its diarrheagenic toxins and producing environmentally-resistant spores necessary for transmission between hosts. These findings provide foundational data for understanding the molecular and genetic basis of how C. difficile growth is inhibited by butyrate and how butyrate alters C. difficile virulence in the face of a highly competitive and dynamic gut environment.

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Expanded CUG repeat RNA alters gene expression profiles in myotonic dystrophy model cells

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GABPα2β2 tetramer deficiency alters transcriptional profiles in NK cells

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