Ontology highlight
ABSTRACT:
PROVIDER: PRJNA886954 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21798800.fastq.gz | Fastqsanger.gz | |||
| SRR21798801.fastq.gz | Fastqsanger.gz | |||
| SRR21798802.fastq.gz | Fastqsanger.gz | |||
| SRR21798803.fastq.gz | Fastqsanger.gz | |||
| SRR21798804.fastq.gz | Fastqsanger.gz |
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Project description:We explore whether a low-energy diet intervention for Metabolic dysfunction-associated steatohepatitis (MASH) improves liver disease by means of modulating the gut microbiome. 16 individuals were given a low-energy diet (880 kcal, consisting of bars, soups, and shakes) for 12 weeks, followed by a stepped re-introduction to whole for an additional 12 weeks. Stool samples were obtained at 0, 12, and 24 weeks for microbiome analysis. Fecal microbiome were measured using 16S rRNA gene sequencing. Positive control (Zymo DNA standard D6305) and negative control (PBS extraction) were included in the sequencing. We found that low-energy diet improved MASH disease without lasting alterations to the gut microbiome.
2024-12-31 | E-MTAB-14061 | biostudies-arrayexpress
Project description:Morphine causes microbial dysbiosis. In this study we focused on restoration of native microbiota in morphine treated mice and looked at the extent of restoration and immunological consequences of this restoration. Fecal transplant has been successfully used clinically, especially for treating C. difficile infection2528. With our expanding knowledge of the central role of microbiome in maintenance of host immune homeostasis17, fecal transplant is gaining importance as a therapy for indications resulting from microbial dysbiosis. There is a major difference between fecal transplant being used for the treatment of C. difficile infection and the conditions described in our studies. The former strategy is based on the argument that microbial dysbiosis caused by disproportionate overgrowth of a pathobiont can be out-competed by re-introducing the missing flora by way of a normal microbiome transplant. This strategy is independent of host factors and systemic effects on the microbial composition. Here, we show that microbial dysbiosis caused due to morphine can be reversed by transplantation of microbiota from the placebo-treated animals.
2016-06-01 | E-MTAB-3723 | biostudies-arrayexpress
Project description:Dietary intake of fruits and vegetables (FV) has been inversely associated with lower risk of ulcerative colitis. A pig model was used to evaluate the impact of feeding FV on the host response to dextran sulfate sodium (DSS)-induced colitis. Methods: Six-week-old pigs were fed a grower diet alone or supplemented with lyophilized FV equivalent to the half (half-FV) or full (full-FV) daily levels recommended for humans by the Dietary Guidelines for Americans (DGA). Pigs were fed a 1) grower diet alone (negative control), 2) grower diet and orally treated with 4% DSS for 10 days to induce colitis (positive control), 3) half-FV diet treated with 4% DSS or 4) full-FV diet treated with 4% DSS. Pigs were monitored for the development of clinical signs of colitis. Proximal colon (PC) contents and mucosa (PCM) were collected for gut metagenome, tissue transcriptome and histopathological analysis. Results: Pigs fed the full-FV diet did not exhibit diarrhea, showed less fecal occult blood (FOB), PCM crypt hyperplasia but with no differential expressed genes (DEG) or changes in PC microbiome diversity (p < 0.05). Pigs within the half-FV group exhibited increased group FOB and DEG associated with tissue remodeling, crypt and goblet cell hyperplasia in the PCM and no changes in PC microbiome diversity and two pigs exhibiting diarrhea (p < 0.05). Pigs within the DSS positive control group exhibited a reduced DEG involved with intestinal immune response and PC microbiome diversity with altered metagenome, increased group PCM erosion and FOB with persistent diarrhea in one pig (p < 0.05) Conclusions: Overall, our results showed that pigs fed a three-week full-FV supplemented diet, were resistant to DSS-induced colitis with a differential dose-dependent protective effect on host intestinal tissue and gut metagenome when exposed to an inflammatory challenge.
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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.
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Project description:Microbiome analysis has relied largely on metagenomics to characterize microbial populations and predict their functions. Here, we used a TMT LC-MSMS metaproteomic analysis of the fecal microbiome in piglets before and after weaning to compare protein abundances as they pertain to microbial populations specific to either a milk- or plant-based diet. Fecal samples were collected from six piglets on the day of weaning and four weeks after transitioning to a standard nursery diet. Using the 12,554 protein groups identified in samples, we confirmed the shift in protein composition that takes place in response to the microbial succession following weaning and demonstrated the redundancy in metabolic processes between taxa. We identified taxa with roles as primary degraders based on corresponding proteins synthesized, thereby providing evidence for cross-feeding. Proteins associated with the breakdown of milk-specific carbohydrates were common among pre-weaned pigs, whereas the proteome of post-weaned piglets contained a greater abundance of proteins involved in the breaking down plant-specific carbohydrates. Furthermore, output revealed that production of propionate takes place via the propionaldehyde pathway in pre-weaned piglets, but changes to production via the succinate pathway in post-weaned piglets. Finally, a disproportionate quantity of carbohydrate-active enzymes (CAZymes) (~8%) were produced by fungi, which typically only represent ~0.1% of the microbiome taxa. Information gathered through this characterization of the metaproteome before and after weaning revealed important differences regarding the role of members in the microbial community, thereby providing information for the optimization of diets and products for both piglet and microbiome health.
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