Gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA725388 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14332000_1.fastq.gz | Fastqsanger.gz | |||
| SRR14332000_2.fastq.gz | Fastqsanger.gz | |||
| SRR14332001_1.fastq.gz | Fastqsanger.gz | |||
| SRR14332001_2.fastq.gz | Fastqsanger.gz | |||
| SRR14332002_1.fastq.gz | Fastqsanger.gz |
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Project description:Gut microbiome research is rapidly moving towards the functional characterization of the microbiota by means of shotgun meta-omics. Here, we selected a cohort of healthy subjects from an indigenous and monitored Sardinian population to analyze their gut microbiota using both shotgun metagenomics and shotgun metaproteomics. We found a considerable divergence between genetic potential and functional activity of the human healthy gut microbiota, in spite of a quite comparable taxonomic structure revealed by the two approaches. Investigation of inter-individual variability of taxonomic features revealed Bacteroides and Akkermansia as remarkably conserved and variable in abundance within the population, respectively. Firmicutes-driven butyrogenesis (mainly due to Faecalibacterium spp.) was shown to be the functional activity with the higher expression rate and the lower inter-individual variability in the study cohort, highlighting the key importance of the biosynthesis of this microbial by-product for the gut homeostasis. The taxon-specific contribution to functional activities and metabolic tasks was also examined, giving insights into the peculiar role of several gut microbiota members in carbohydrate metabolism (including polysaccharide degradation, glycan transport, glycolysis and short-chain fatty acid production). In conclusion, our results provide useful indications regarding the main functions actively exerted by the gut microbiota members of a healthy human cohort, and support metaproteomics as a valuable approach to investigate the functional role of the gut microbiota in health and disease.
2017-07-19 | PXD005780 | Pride
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2020-02-27 | E-MTAB-8798 | biostudies-arrayexpress
Project description:This study aims to elucidate the impact of gut microbiota alterations on tumorigenesis and immune response in lung adenocarcinoma (LUAD). Using Gprc5a-/- mice as a model, we performed fecal microbiota transfer (FMT) from Gprc5a-/- and Gprc5a-/-; Lcn2-/- donors to investigate the role of gut microbiome changes in modulating tumor growth and the immune microenvironment. Single-cell RNA sequencing (scRNA-seq) was conducted on colonic lamina propria and subcutaneous tumor tissues. Our findings demonstrate that gut microbiota from Lcn2-deficient mice promotes systemic inflammation and immunosuppression, enhancing tumor progression. This study provides insights into the microbiome's influence on LUAD and potential therapeutic strategies targeting microbiome-related pathways.
2024-09-12 | GSE271872 | GEO
Project description:<p>Emerging evidence that the gut microbiota may contribute in important ways to human health and disease has led us and others to hypothesize that both symbiotic and pathological relationships between gut microbes and their host may be key contributors to obesity and the metabolic complications of obesity. Our "Thrifty Microbiome Hypothesis" poses that gut microbiota play a key role in human energy homeostasis. Specifically, constituents of the gut microbial community may introduce a survival advantage to its host in times of nutrient scarcity, promoting positive energy balance by increasing efficiency of nutrient absorption and improving metabolic efficiency and energy storage. However, in the presence of excess nutrients, fat accretion and obesity may result, and in genetically predisposed individuals, increased fat mass may result in preferential abdominal obesity, ectopic fat deposition (liver, muscle), and metabolic complications of obesity (insulin resistance, hypertension, hyperlipidemia). Furthermore, in the presence of excess nutrients, a pathological transition of the gut microbial community may occur, causing leakage of bacterial products into the intestinal lymphatics and portal circulation, thereby inducing an inflammatory state, further aggravating metabolic syndrome traits and accelerating atherosclerosis. This pathological transition and the extent to which antimicrobial leakage occurs and causes inflammatory and other maladaptive sequelae of obesity may also be influenced by host factors, including genetics. In the proposed study, we will directly test the Thrifty Microbiome Hypothesis by performing detailed genomic and functional assessment of gut microbial communities in intensively phenotyped and genotyped human subjects before and after intentional manipulation of the gut microbiome. To address these hypotheses, five specific aims are proposed: (1) enroll three age- and sex-matched groups from the Old Order Amish: (i) 50 obese subjects (BMI > 30 kg/m2) with metabolic syndrome, (ii) 50 obese subjects (BMI > 30 kg/m2) without metabolic syndrome, and (iii) 50 non-obese subjects (BMI < 25 kg/m2) without metabolic syndrome and characterize the architecture of the gut microbiota from the subjects enrolled in this study by high-throughput sequencing of 16S rRNA genes; (2) characterize the gene content (metagenome) to assess the metabolic potential of the gut microbiota in 75 subjects to determine whether particular genes or pathways are correlated with disease phenotype; (3) characterize the transcriptome in 75 subjects to determine whether differences in gene expression in the gut microbiota are correlated with disease phenotype, (4) determine the effect of manipulation of the gut microbiota with antibiotics on energy homeostasis, inflammation markers, and metabolic syndrome traits in 50 obese subjects with metabolic syndrome and (5) study the relationship between gut microbiota and metabolic and cardiovascular disease traits, weight change, and host genomics in 1,000 Amish already characterized for these traits and in whom 500K Affymetrix SNP chips have already been completed. These studies will provide our deepest understanding to date of the role of gut microbes in terms of 'who's there?', 'what are they doing?', and 'how are they influencing host energy homeostasis, obesity and its metabolic complications? PUBLIC HEALTH RELEVANCE: This study aims to unravel the contribution of the bacteria that normally inhabit the human gastrointestinal tract to the development of obesity, and its more severe metabolic consequences including cardiovascular disease, insulin resistance and Type II diabetes. We will take a multidisciplinary approach to study changes in the structure and function of gut microbial communities in three sets of Old Order Amish patients from Lancaster, Pennsylvania: obese patients, obese patients with metabolic syndrome and non-obese individuals. The Old Order Amish are a genetically closed homogeneous Caucasian population of Central European ancestry ideal for genetic studies. These works have the potential to provide new mechanistic insights into the role of gut microflora in obesity and metabolic syndrome, a disease that is responsible for significant morbidity in the adult population, and may ultimately lead to novel approaches for prevention and treatment of this disorder.</p>
| phs000258 | dbGaP
Project description:Interventions: Colorectal adenoma (excessive syndrome: intestinal damp-heat syndrome) group:None;Colorectal adenoma (deficiency syndrome: spleen and stomach deficiency syndrome) group:None;Colorectal cancer (excessive syndrome: damp-heat accumulation syndrome) group:None;Colorectal cancer (deficiency syndrome: spleen deficiency and qi stagnation syndrome) group:None;Healthy control group:None
Primary outcome(s): Gut microbiota
Study Design: Factorial
| 2741054 | ecrin-mdr-crc
Project description:Polycystic ovary syndrome (PCOS) is a multifactorial disorder closely associated with metabolic dysfunction, yet the contribution of gut microbiota–derived metabolites remains incompletely understood.
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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.
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