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Transcriptomic and lipidomic analyses unravel the responses of Faecalibacterium prausnitzii to calcium palmitate

ABSTRACT: We investigate the underlying mechanism of the CP inhibition on F. prausnitzii by analysing its effects at the transcriptomic and lipidomic levels.

ORGANISM(S): Faecalibacterium prausnitzii

PROVIDER: GSE225701 | GEO | 2024/03/01

REPOSITORIES: GEO

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Transcriptomic and lipidomic analysis unravels the response of Faecalibacterium prausnitzii to calcium palmitate

Project description:Infant formula is a suggested alternative to human milk if breastfeeding is not an option; vegetable oil blends are commonly used in infant formula (IF) to replace dairy fat, which can induce the formation of the poorly soluble soap calcium palmitate (CP) in the infant’s gut. Previously, we observed that CP at a low concentration of 0.01 mg/ml inhibits the growth of dominant infant bacteria such as Faecalibacterium prausnitzii both during the exponential phase as well as in the stationary phase. Here, we investigate the underlying mechanism of the CP inhibition on infant-gut bacteria using F. prausnitzii as a model by analysing its growth at a transcriptomic and lipidomic level.

2021-11-12 | ST001987 | MetabolomicsWorkbench

Faecalibacterium prausnitzii abrogates immunotherapy toxicity

Project description:To elucidate whether Faecalibacterium prausnitzii has effects on intestinal toxicity induced by immune checkpoint inhibitors, we performed RNA-seq analysis of colon tissues of mice receiving DSS, DSS+ICB and DSS+ICB+F. prausnitzii gavage to compare the gene expression profiles.

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Anti-inflammatory Effects of the Commensal Bacterium Faecalibacterium prausnitzii analyzed by microarrays

Project description:The human intestinal microbiota plays an essential role in host health. Modifications in its composition and diversity could induce pathologies such as inflammatory bowel diseases (IBD). These diseases are characterized by an unbalanced intestinal microbiota (a process known as dysbiosis) and an altered immune response. Faecalibacterium prausnitzii, the most abundant commensal bacterium in the human intestinal microbiota of healthy individuals (representing more than 5% of the total bacterial population), has been reported to be lower in feces and mucosa-associated microbiota of IBD patients. In addition, we have shown that both F. prausnitzii and its culture supernatant (SN) have anti-inflammatory and protective effects in both acute and chronic colitis models. However, the host molecular mechanisms involved in these anti-inflammatory effects remain unknown. In order to address this issue, we performed DNA chip-based transcriptomic analyses in HT-29 human intestinal epithelial cells stimulated with TNF-a and exposed to F. prausnitzii SN or to BHI (growth medium for F prausnitzii).

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An integrative multi-omics approach to characterize prebiotic inulin effects on Faecalibacterium prausnitzii

Project description:Faecalibacterium prausnitzii, a major commensal bacterium in the human gut, is well known for its anti-inflammatory effects, which improve host intestinal health. Although several studies have reported that inulin, a well-known prebiotic, increases the abundance of F. prausnitzii in the intestine, the mechanism underlying this effect remains unclear. In this study, we applied liquid chromatography tandem mass spectrometry (LC-MS/MS)-based multi-omics approaches to identify biological and enzymatic mechanisms of F. prausnitzii involved in the selective digestion of inulin. An LC-MS/MS-based intracellular proteomic and metabolic profiling was performed to determine the quantitative changes in specific proteins and metabolites of F. prausnitzii when grown on inulin. Interestingly, proteomic analysis revealed that the putative proteins involved in inulin-type fructan utilization by F. prausnitzii, particularly b-fructosidase and amylosucrase were upregulated in the presence of inulin. To investigate the function of these proteins, we overexpressed bfrA and ams, genes encoding beta-fructosidase and amylosucrase, respectively, in Escherichia coli, and observed their ability to degrade fructan. In addition, the enzyme activity assay demonstrated that intracellular fructan hydrolases degrade the inulin-type fructans taken up by fructan ATP-binding cassette transporters. Furthermore, we showed that the fructose uptake activity of F. prausnitzii was enhanced by the fructose phosphotransferase system transporter when inulin was used as a carbon source.

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