Human gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA636933 | ENA |
REPOSITORIES: ENA
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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.
2021-12-31 | GSE189233 | GEO
Project description:This study investigated whether dietary poricoic acid A (PAA) alleviates chronic unpredictable stress (CUS)-induced depressive-like behaviors in mice by modulating the gut microbiota-immune axis. Male C57BL/6J mice were subjected to CUS and treated with PAA. Results showed that PAA alleviated depressive- and anxiety-like behaviors, reduced hippocampal neuronal damage, and restored gut microbiota composition by suppressing harmful bacteria like Ligilactobacillus murinus while promoting beneficial taxa such as Akkermansia muciniphila and Lactobacillus reuteri. Hippocampal transcriptomics revealed that PAA modulated immune cell infiltration by reducing M1 and restoring M2 macrophages, with significant correlations between gut microbial taxa and hippocampal immune gene expression. Functional analyses indicated that PAA regulated pathways related to synaptic plasticity and neuroinflammation, which was confirmed by qPCR and Western blot showing restored expression of HSP90B1, RPS6KB2, IGF2BP2, and COL4A5. In conclusion, dietary PAA alleviates depressive-like behaviors in CUS mice by remodeling the gut microbiota and modulating the hippocampal M1/M2 macrophage balance via the gut-brain axis, supporting its potential as a prebiotic-like nutritional agent for major depressive disorder.
2026-08-05 | GSE327915 | GEO
Project description:Accumulating evidence demonstrates that the gut microbiota affects brain function and behavior, including depressive behavior. Antidepressants are the main drugs used for treatment of depression. We hypothesized that antidepressant treatment could modify gut microbiota which can partially mediate their antidepressant effects. Mice were chronically treated with one of five antidepressants (fluoxetine, escitalopram, venlafaxine, duloxetine or desipramine), and gut microbiota was analyzed, using 16s rRNA gene sequencing. After characterization of differences in the microbiota, chosen bacterial species were supplemented to vehicle and antidepressant-treated mice, and depressive-like behavior was assessed to determine bacterial effects. RNA-seq analysis was performed to determine effects of bacterial treatment in the brain. Antidepressants reduced richness and increased beta diversity of gut bacteria, compared to controls. At the genus level, antidepressants reduced abundances of Ruminococcus, Adlercreutzia, and an unclassified Alphaproteobacteria. To examine implications of the dysregulated bacteria, we chose one of antidepressants (duloxetine) and investigated if its antidepressive effects can be attenuated by simultaneous treatment with Ruminococcus flavefaciens or Adlercreutzia equolifaciens. Supplementation with R. flavefaciens diminished duloxetine-induced decrease in depressive-like behavior, while A. equolifaciens had no such effect. R. flavefaciens treatment induced changes in cortical gene expression, up-regulating genes involved in mitochondrial oxidative phosphorylation, while down-regulating genes involved in neuronal plasticity. Our results demonstrate that various types of antidepressants alter gut microbiota composition, and further implicate a role for R. flavefaciens in alleviating depressive-like behavior.
2019-04-05 | GSE129359 | GEO
Project description:Irritable Bowel Syndrome (IBS) is a disorder of the gut-brain axis, characterized by altered gut function and frequent psychiatric co-morbidity. Although altered intestinal microbiome profiles have been documented, their relevance to the clinical expression of IBS is unknown. To evaluate a functional role of the microbiota, we colonized germ-free mice with fecal microbiota from healthy controls or IBS patients with accompanying anxiety, and monitored gut function and behavior. Mouse microbiota profiles clustered according to their human donors. Despite having taxonomically similar composition as controls, mice with IBS microbiota had distinct serum metabolomic profiles related to neuro- and immunomodulation. Mice with IBS, but not control microbiota, exhibited faster gastrointestinal transit, intestinal barrier dysfunction, innate immune activation and anxiety-like behavior. These results support the notion that the microbiota contributes to both intestinal and behavioral manifestations of IBS and rationalize the use of microbiota-directed therapies in ameliorating IBS.
2017-03-02 | GSE61841 | GEO
Project description:Peripartum depression can have severe impact on the mother’s and the infant’s health. Yet, its biological underpinnings are largely unknown. The present study sought to identify transcriptomic signatures of depressive symptoms during pregnancy and postpartum. Blood samples were collected during late pregnancy or early postpartum for mRNA isolation and sequencing, while depressive symptoms were assessed using the Edinburgh Postnatal Depression Scale. Stratifying according to the timepoint samples were collected, differentially expressed genes (DEGs) were identified by (1) comparing mRNA levels between the symptom trajectory groups, and (2) correlating with EPDS scores. DEGs for samples collected late pregnancy, but not postpartum, were associated with depressive symptoms occurring only during pregnancy or persisting postpartum, compared with controls. There were 16 upregulated and 109 downregulated DEGs significantly associated with changes in EPDS score at week 32 among samples collected late pregnancy. Gene Set Enrichment Analysis identified immune response and cell motility as processes linked to these DEGs. Hypothesis-based analysis on previously identified postpartum depressive symptoms-related DEGs, replicated a positive association between expression of immune-related genes ISG15 and RSAD2 with postpartum-onset depressive symptoms, both at samples taken during late pregnancy and postpartum. The present findings point to transcriptomic signatures associated with depressive symptoms, mostly related to immune system dysregulation.
2025-09-24 | GSE290313 | GEO
Project description:Background: Osteoarthritis (OA) is a globally prevalent degenerative joint disorder that imposes significant socioeconomic burdens. While traditionally viewed as a localized “wear-and-tear” disease, emerging evidence supports a systemic pathogenesis involving the gut-joint axis. The oral-gut-joint pathway remains underexplored in OA pathophysiology. Objective: This study aimed to characterize oral and gut microbiota signatures in knee OA patients and elucidate their functional connections to cartilage degeneration through multiomics integration. Methods: We conducted a cross-sectional observational study involving 25 OA patients and 20 healthy controls. 16S rDNA gene amplicon sequencing region was performed on fecal and oropharyngeal swab samples. Cartilage tissues were subjected to transcriptomic and proteomic analyses. Results: We identified distinct dysbiosis patterns in both the gut and oral microbiomes of OA patients. The α-Diversity of the gut microbiota significantly increased (P < 0.05) with enrichment of Ruminococcaceae and Subdoligranulum. Concurrently, the oral microbiota showed increased α-Diversity and activation of the lipopolysaccharide biosynthesis pathway. We constructed two significant cross-omics correlation modules: one linking gut microbes (Lachnospiraceae and Muribaculaceae) to cartilage inflammatory genes (MAPK11, ITGB3, CD55 and ANGPT2) and extracellular matrix remodelling proteins and another connecting gut microbes (Helicobacter, Pseudomonas, and Phocea) with CXCL14 and GNGT2. Conclusion: Our study revealed the dysbiotic characteristics of the oral-gut microbiome and its complex functional connections with pathological changes in cartilage. These findings offer novel mechanistic insights and potential therapeutic targets for microbiota-based precision interventions in OA.
2026-05-27 | GSE331536 | GEO
Project description:The larynx is essential for swallowing, breathing, coughing, and voice production, supported by its unique microbial and immunological environment. Our previous research highlighted the role of resident laryngeal microbiota in shaping local immune responses. With growing interest in the gut-lung axis—the bidirectional communication between gut and respiratory immunity—the potential influence of gut microbiota on laryngeal immunity warrants exploration. We hypothesized that a gut-larynx axis may exist, where both resident laryngeal and gut microbiota contribute to immune modulation in the larynx. To investigate this, we treated conventionally raised, wild-type C57BL/6J mice with an oral antibiotic regimen known to disrupt gut microbiota, comparing them to untreated controls. Following treatment, the gut microbiota was significantly disrupted, while the laryngeal microbiota remained largely unchanged. However, antibiotic-treated mice exhibited marked changes in epithelial and immune cell proportions, as well as fibroblasts. Differential gene expression across cell types highlighted pathways related to epithelial barrier integrity, immune signaling, and bacterial response. Additionally, gut dysbiosis affected gene regulatory networks, with the activity of regulons Etv4(+), Irf3(+), Hltf(+), Mga(+), and Nfil3(+) showing significant changes. Notably, cell-cell communication was also altered, especially in immune-epithelial interactions, with integrin-mediated signaling emerging as a key ligand-receptor pathway in these intercellular communications. These findings suggest that gut and laryngeal microbiota may work synergistically to modulate immune responses in the larynx, underscoring the importance of considering gut-larynx interactions in studies of respiratory immunity.
2025-03-04 | GSE290718 | GEO
Project description:In this study we investigated whether gut microbiota profile of Italian healthy volunteers could differ based on their geaographical origin. To this purpose, fecal samples were collected from 31 healthy individuals living in 3 different italian regions (Lombardy, North; Lazio, Center; Apulia, South) and their respective microbiota profiles were analyzed employing 16S metagenomic sequencing method. This study identifies differences in the gut microbiota content and richness among individuals with the same ethnicity coming from three different Italian regions.
2026-01-08 | E-MTAB-8136 | biostudies-arrayexpress
Project description:In this study, we performed a comparative analysis of gut microbiota composition and gut microbiome-derived bacterial extracellular vesicles (bEVs) isolated from patients with solid tumours and healthy controls. After isolating bEVs from the faeces of solid tumour patients and healthy controls, we performed spectrometry analysis of their proteomes and next-generation sequencing (NGS) of the 16S gene. We also investigated the gut microbiomes of faeces from patientsand controls using 16S rRNA sequencing. Machine learning was used to classify the samples into patients and controls based on their bEVs and faecal microbiomes.
2024-08-08 | PXD047510 | Pride