Gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA749141 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR15221300_1.fastq.gz | Fastqsanger.gz | |||
| SRR15221300_2.fastq.gz | Fastqsanger.gz | |||
| SRR15221301_1.fastq.gz | Fastqsanger.gz | |||
| SRR15221301_2.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
Project description:Opioids such as morphine have many beneficial properties as analgesics, however, opioids may induce multiple adverse gastrointestinal symptoms. We have recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. However, it is unclear how opioids modulate the gut homeostasis. By using a mouse model of morphine treatment, we studied effects of morphine treatment on gut microbiome. We characterized phylogenetic profiles of gut microbes, and found a significant shift in the gut microbiome and increase of pathogenic bacteria following morphine treatment when compared to placebo. In the present study, wild type mice (C57BL/6J) were implanted with placebo, morphine pellets subcutaneously. Fecal matter were taken for bacterial 16s rDNA sequencing analysis at day 3 post treatment. A scatter plot based on an unweighted UniFrac distance matrics obtained from the sequences at OTU level with 97% similarity showed a distinct clustering of the community composition between the morphine and placebo treated groups. By using the chao1 index to evaluate alpha diversity (that is diversity within a group) and using unweighted UniFrac distance to evaluate beta diversity (that is diversity between groups, comparing microbial community based on compositional structures), we found that morphine treatment results in a significant decrease in alpha diversity and shift in fecal microbiome at day 3 post treatment compared to placebo treatment. Taxonomical analysis showed that morphine treatment results in a significant increase of potential pathogenic bacteria. Our study shed light on effects of morphine on the gut microbiome, and its role in the gut homeostasis.
2018-04-16 | E-MTAB-5546 | biostudies-arrayexpress
Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
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Project description:This study demonstrates the usefulness of the API by generating a baseline gut microbiota profile of a healthy population and estimating reference intervals for the functional abundance of manually selected KEGG pathways. API facilitates microbiome research by providing dynamic and customizable tools for estimating reference intervals for gut microbiota functional abundances. Through the API, researchers can rapidly generate gut microbiota functional profiles of healthy populations to use as a baseline for comparison. The API also allows users to manually select specific KEGG pathways and estimate reference intervals for the functional abundance of those pathways. By generating these customized reference intervals, researchers can better understand the expected range of gut microbiota functions in healthy individuals. API enables microbiome studies to go beyond simple taxonomic profiling and delve deeper into the functional potential of gut microbiome communities. In summary, API represents a valuable tool for microbiome researchers that enhances the ability to elucidate connections between gut microbial functions and human health.
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Project description:Koala Retrovirus-A is a gamma-retrovirus sweeping wild koalas via a combination of horizontal and vertical transfer, contributing substantial genomic diversity across and even within koala populations. While studies have estimated KoRV-A's integration into the koala genome occurred 120–50,000 years ago, the origin and spread patterns of its endogenization remain unclear. Here, we analyze KoRV-A germline insertions using whole-genome sequencing data from 405 wild koalas, encompassing nearly the full koala habitat range. We map a trajectory of KoRV-A evolution and propose that KoRV-A first entered the koala germline genome near Coffs Harbour. As KoRV-A spread, replication-competitive subtypes emerged, two of which recombined with an ancient endogenous retrovirus, PhER, resulting in distinct recombination variants across northern and southern koala populations. Additionally, we identified a geographic barrier north of Sydney, which has slowed the southward spread of KoRV-A into Sydney and beyond.
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