1054 Flemish Gut Flora Project (FGFP) samples (16S sequencing, dual index)
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ABSTRACT:
PROVIDER: EGAS00001003296 | EGA |
REPOSITORIES: EGA
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Project description:Study exploring the neuroactive potential of the human gut microbiota in relation to quality of life and depression. This dataset includes shotgun sequenced samples from the FGFP (Flemish Gut Flora Project: N=150) and TR-MDD (Treatment-Resistant Major Depression Disorder: N=7). Samples were provided by volunteers from the Flanders region in Belgium, and the dataset is balanced for age, gender, and stool consistency.
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Project description:Major depressive disorder is caused by gene-environment interactions and the gut microbiota plays a pivotal role in the development of depression. However, the mechanisms by which the gut microbiota modulates depression remain elusive. Herein, we detected the differentially expressed hippocampal long non-coding RNAs (lncRNAs), messenger RNAs (mRNAs) and microRNAs (miRNAs) between mice inoculated with gut microbiota from major depressive disorder patients or healthy controls, to identify the effects of gut microbiota-dysbiosis on gene regulation patterns at the transcriptome level. We also performed functional analysis to explore the microbial-regulated pathological mechanisms of depression. Two hundred mRNAs, 358 lncRNAs and 4 miRNAs were differentially expressed between the two groups. Functional analysis of these differentially expressed mRNAs indicated dysregulated inflammatory response to be the primary pathological change. Intersecting the differentially expressed mRNAs with targets of differentially expressed miRNAs identified 47 intersected mRNAs, which were mainly related to neurodevelopment. Additionally, we constructed a microbial-regulated lncRNA-miRNA-mRNA network based on RNA-RNA interactions. According to the competitive endogenous RNA hypothesis, two neurodevelopmental ceRNA sub-networks implicating in depression were identified. This study provides new understanding of the pathogenesis of depression induced by gut microbiota-dysbiosis and may act as a theoretical basis for the development of gut microbiota-based antidepressants.
2021-12-31 | GSE189159 | GEO
Project description:Major depressive disorder is caused by gene-environment interactions and the gut microbiota plays a pivotal role in the development of depression. However, the mechanisms by which the gut microbiota modulates depression remain elusive. Herein, we detected the differentially expressed hippocampal long non-coding RNAs (lncRNAs), messenger RNAs (mRNAs) and microRNAs (miRNAs) between mice inoculated with gut microbiota from major depressive disorder patients or healthy controls, to identify the effects of gut microbiota-dysbiosis on gene regulation patterns at the transcriptome level. We also performed functional analysis to explore the microbial-regulated pathological mechanisms of depression. Two hundred mRNAs, 358 lncRNAs and 4 miRNAs were differentially expressed between the two groups. Functional analysis of these differentially expressed mRNAs indicated dysregulated inflammatory response to be the primary pathological change. Intersecting the differentially expressed mRNAs with targets of differentially expressed miRNAs identified 47 intersected mRNAs, which were mainly related to neurodevelopment. Additionally, we constructed a microbial-regulated lncRNA-miRNA-mRNA network based on RNA-RNA interactions. According to the competitive endogenous RNA hypothesis, two neurodevelopmental ceRNA sub-networks implicating in depression were identified. This study provides new understanding of the pathogenesis of depression induced by gut microbiota-dysbiosis and may act as a theoretical basis for the development of gut microbiota-based antidepressants.
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Project description:Purpose: Gut microbiota is associated with the progression of brain tumor. However, the alterations in the gut microbiota during glioma growth and temozolomide (TMZ) therapy remains to be understood. Methods: C57BL/6 male mice were implanted with GL261 glioma cells. TMZ/sodium carboxymethyl cellulose (SCC) was administered by gavage for five consecutive days (from 8 to 12 days after implantation). Fecal samples were collected before (T0) and on days 7 (T1), 14 (T2), and 28 (T3) after implantation. The gut microbiota was analyzed using 16S ribosomal DNA sequencing followed by absolute and relative quantitation analyses. Results: Nineteen genera were altered during glioma progression with the most dramatic changes in Firmicutes and Bacteroidetes phyla. During glioma growth, Lactobacillus abundance decreased at the earlier stage of glioma development (T1), and then gradually increased (T2, T3); Intestinimonas abundance exhibited a persistent increase; Anaerotruncus showed a transient increase and then a subsequent decrease. Twenty genera altered following TMZ treatment. The enrichment of Akkermansia and Bifidobacterium was observed only at the early stage following TMZ treatment (T2), but not at the later stage (T3). Additionally, the decrease of Anaerotruncus was slighter in TMZ group at T3 comparing to the vehicle group. The abundance of Intestinimonas increased constantly during the progression of glioma, but was unaffected by TMZ. Conclusions: Glioma development and progression resulted in altered gut microbiota. TMZ reversed the decrease of Anaerotruncus in glioma at T3, and increased the abundance of Bifidobacterium with no influence on the increase of Intestinimonas. Short-term and long-term effects of TMZ treatment on the bacterial communities may be differential. This study will improve understanding the role of gut microbiota in glioma, and help develop gut microbiota as a potential therapeutic target.
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Project description:Chronic acid suppression by proton pump inhibitor (PPI) has been hypothesized to alter the gut microbiota via a change in intestinal pH. To evaluate the changes in gut microbiota composition by long-term PPI treatment.
2015-04-14 | GSE67800 | GEO