Ontology highlight
ABSTRACT:
PROVIDER: PRJNA818258 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18456338_1.fastq.gz | Fastqsanger.gz | |||
| SRR18456338_2.fastq.gz | Fastqsanger.gz | |||
| SRR18456339_1.fastq.gz | Fastqsanger.gz | |||
| SRR18456339_2.fastq.gz | Fastqsanger.gz | |||
| SRR18456340_1.fastq.gz | Fastqsanger.gz |
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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.
2018-04-16 | E-MTAB-5546 | biostudies-arrayexpress
Project description:We have previously reported human gastrin overexpressing transgenic mice (=INS-GAS mice) and Helicobacter felis (=H.felis) infection synergistically accelerated gastric cancer in mice stomachs. (Wang et al 2000) Using this mouse model, we employed microarray analysis of gene expression profiling to identify gastric cancer-specific genes. Experiment Overall Design: 30 male INS-GAS mice (FVB/N background) were divided into groups: 15 mice were infected with H.felis at the age of 2-3 months and another 15 mice were not infected. 30 male non-transgenic FVB/N mice were also divided into 2 groups: 15 mice were infected with H.felis at the age of 2-3 months and another 15 mice were not infected. All mice were sacrificed after 6 months of H.felis infection, and total RNAs were extracted from whole stomachs. Experiment Overall Design: Histological analysis confirmed all of the stomachs in H.felis infected INS-GAS mice (=INSGAS+Hf) had intra-epithelial gastric cancer, and some of them also had invasion into submucosa, but none of them had distant metastatic lesions. Other 3 control groups had following histology in stomachs. (1) non-transgenic mice with H.felis infection (=FVB+Hf): severe intestinal metaplasia and/or mild dysplasia. (2) INS-GAS mice without infection (=INSGAS wt): severe atrophic gastritis and/or mild intestinal metaplasia (3) non-transgenic mice without infection (=FVB wt): normal stomach. Total RNAs extracted from each mouse in 4 different groups were used for microarray analysis of Affymetrix GeneChip. Experiment Overall Design: Up- or down-regulated genes in INSGAS+Hf group compared with all 3 control groups (FVB+HF, INSGAS wt and FVB wt) may represent gastric cancer-specific genes.
2008-06-13 | E-GEOD-4651 | biostudies-arrayexpress
Project description:We have previously reported human gastrin overexpressing transgenic mice (=INS-GAS mice) and Helicobacter felis (=H.felis) infection synergistically accelerated gastric cancer in mice stomachs. (Wang et al 2000) Using this mouse model, we employed microarray analysis of gene expression profiling to identify gastric cancer-specific genes. Keywords: disease state analysis
2006-04-13 | GSE4651 | GEO
Project description:We are now trying to elucidate the mechanism of Helicobacter-induced gastritis and gastric cancer. To identify genes involved in these Helicobacter-associated diseases, we infected Helicobacter felis to INS-GAS (insulin-gastrin transgenic) mice (C57BL/6 background) which shows accelerated development of gastritis and gastric cancer.
2011-02-17 | GSE27361 | GEO
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2013-10-30 | GSE51592 | GEO
Project description:HIV is known to severely affect the gastrointestinal immune system, in particular compartments of immunity that regulate gut microbial composition. Furthermore, recent studies in mice have shown that dysregulation of the gut microbiome can contribute to chronic inflammation, which is a hallmark of HIV and is thought to fuel disease progression. We sought to understand whether the gut microbial community differs in HIV-infected subjects, and whether such putative differences are associated with disease progression. We found that dysbiosis in the gut mucosally-adherent bacterial community associates with markers of chronic inflammation and disease progression in HIV-infected subjects, and this dysbiosis remains in many subjects undergiong antiretroviral therapy.
2013-07-10 | GSE43746 | GEO
Project description:HIV is known to severely affect the gastrointestinal immune system, in particular compartments of immunity that regulate gut microbial composition. Furthermore, recent studies in mice have shown that dysregulation of the gut microbiome can contribute to chronic inflammation, which is a hallmark of HIV and is thought to fuel disease progression. We sought to understand whether the gut microbial community differs in HIV-infected subjects, and whether such putative differences are associated with disease progression. We found that dysbiosis in the gut mucosally-adherent bacterial community associates with markers of chronic inflammation and disease progression in HIV-infected subjects, and this dysbiosis remains in many subjects undergiong antiretroviral therapy. We used G3 PhyloChip microarrays (commercially available from Second Genome, Inc.) to profile gut bacteria in rectosigmoid biopsies from 32 subjects: 6 HIV-infected viremic untreated (VU), 18 HIV-infected subjects on highly active antiretroviral therapy (HAART), 1 HIV-infected long-term non-progressor that is untreated (LTNP), and 9 HIV-uninfected subjects (HIV-).
2013-07-10 | E-GEOD-43746 | biostudies-arrayexpress
Project description:Soil transplant serves as a proxy to simulate climate change in realistic climate regimes. Here, we assessed the effects of climate warming and cooling on soil microbial communities, which are key drivers in EarthM-bM-^@M-^Ys biogeochemical cycles, four years after soil transplant over large transects from northern (N site) to central (NC site) and southern China (NS site) and vice versa. Four years after soil transplant, soil nitrogen components, microbial biomass, community phylogenetic and functional structures were altered. Microbial functional diversity, measured by a metagenomic tool named GeoChip, and phylogenetic diversity are increased with temperature, while microbial biomass were similar or decreased. Nevertheless, the effects of climate change was overridden by maize cropping, underscoring the need to disentangle them in research. Mantel tests and canonical correspondence analysis (CCA) demonstrated that vegetation, climatic factors (e.g., temperature and precipitation), soil nitrogen components and CO2 efflux were significantly correlated to the microbial community composition. Further investigation unveiled strong correlations between carbon cycling genes and CO2 efflux in bare soil but not cropped soil, and between nitrogen cycling genes and nitrification, which provides mechanistic understanding of these microbe-mediated processes and empowers an interesting possibility of incorporating bacterial gene abundance in greenhouse gas emission modeling. Fifty four samples were collected from three soil types (Phaeozem,Cambisol,Acrisol) in three sites (Hailun, Fengqiu and Yingtan) along a latitude with reciprocal transplant; Both with and without maize cropping in each site; Three replicates in every treatments.
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Project description:Long-term dietary intake influences the structure and activity of the trillions of microorganisms residing in the human gut, but it remains unclear how rapidly and reproducibly the human gut microbiome responds to short-term macronutrient change. Here we show that the short-term consumption of diets composed entirely of animal or plant products alters microbial community structure and overwhelms inter-individual differences in microbial gene expression. The animal-based diet increased the abundance of bile-tolerant microorganisms (Alistipes, Bilophila and Bacteroides) and decreased the levels of Firmicutes that metabolize dietary plant polysaccharides (Roseburia, Eubacterium rectale and Ruminococcus bromii). Microbial activity mirrored differences between herbivorous and carnivorous mammals, reflecting trade-offs between carbohydrate and protein fermentation. Foodborne microbes from both diets transiently colonized the gut, including bacteria, fungi and even viruses. Finally, increases in the abundance and activity of Bilophila wadsworthia on the animal-based diet support a link between dietary fat, bile acids and the outgrowth of microorganisms capable of triggering inflammatory bowel disease. In concert, these results demonstrate that the gut microbiome can rapidly respond to altered diet, potentially facilitating the diversity of human dietary lifestyles. RNA-Seq analysis of the human gut microbiome during consumption of a plant- or animal-based diet.
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Project description:Background: More than 100 million Americans are living with metabolic syndrome, increasing their propensity to develop heart disease– the leading cause of death worldwide. A major contributing factor to this epidemic is caloric excess, often a result of consuming low cost, high calorie fast food. Several recent seminal studies have demonstrated the pivotal role of gut microbes contributing to cardiovascular disease in a diet-dependent manner. Given the central contributions of diet and gut microbiota to cardiometabolic disease, we hypothesized that novel microbial metabolites originating postprandially after fast food consumption may contribute to cardiometabolic disease progression. Methods: To test this hypothesis, we gave conventionally raised or antibiotic-treated mice a single oral gavage of a fast food slurry or a control rodent chow diet slurry and sacrificed the mice four hours later. Here, we coupled untargeted metabolomics in portal and peripheral blood, 16S rRNA gene sequencing, targeted liver metabolomics, and host liver RNA sequencing to identify novel fast food-derived microbial metabolites. Results: We successfully identified several metabolites that were enriched in portal blood, increased by fast food feeding, and essentially absent in antibiotic-treated mice. Strikingly, just four hours post-gavage, we found that fast food consumption resulted in rapid reorganization of the gut microbial community structure and drastically altered hepatic gene expression. Importantly, diet-driven reshaping of the microbiome and liver transcriptome was dependent on a non-antibiotic ablated gut microbial community. Conclusions: Collectively, these data suggest that single fast food meal is sufficient to reshape the gut microbial community yielding a unique signature of food-derived microbial metabolites. Future studies are warranted to determine if these metabolites are causally linked to cardiometabolic disease.
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