Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1148691 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30284200_1.fastq.gz | Fastqsanger.gz | |||
| SRR30284200_2.fastq.gz | Fastqsanger.gz | |||
| SRR30284300_1.fastq.gz | Fastqsanger.gz | |||
| SRR30284300_2.fastq.gz | Fastqsanger.gz | |||
| SRR30284201_1.fastq.gz | Fastqsanger.gz |
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Project description:Erythromycin (ERY) is a commonly used antibiotic that can be found in wastewater effluents globally. Due to the mechanisms by which they kill and prevent bacterial growth, antibiotics can have significant unwanted impacts on the fish gut microbiome. The overall objective of this project was to assess the effects of erythromycin and an antibiotic mixture on fish gut microbiomes. The project was split into two experiments to assess gut microbiome in response to exposure with ERY alone or in mixture with other common antibiotics. The objectives of experiment 1 were to understand uptake and depuration of ERY in juvenile rainbow trout (RBT) over a 7 d uptake followed by a 7 d depuration period using three concentrations of ERY. Furthermore, throughout the study changes in gut microbiome response were assessed. In experiment 2, a follow-up study was conducted using an identical experimental design to assess the impacts of an antibiotic-mixture (ERY, ampicillin, metronidazole, and ciprofloxacin at 100 µg/g each). Here, three matrices were analyzed, with gut collected for 16s metabarcoding, plasma for untargeted metabolomics, and brain for mRNA-seq analysis. ERY was depurated from the fish relatively quickly and gut microbiome dysbiosis was observed at 7 d after exposure, with a slight recovery after the 7 d depuration period. A greater number of plasma metabolites was dysregulated at 14 d compared to 7 d revealing temporality compared to gut microbiome dysbiosis. Furthermore, several transformation products of antibiotics and biomarker metabolites were observed in plasma due to antibiotic exposure. Brain transcriptome revealed only slight alterations due to antibiotic exposure. The results of these studies will help inform aquaculture practitioners and risk assessors when assessing the potential impacts of antibiotics in fish feed and the environment, with implications for host health.
2024-02-07 | GSE253746 | GEO
Project description:Phylogenomics of endemic Australian Ulopinae (Hemiptera: Cicadomorpha: Cicadellidae)
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Project description:The gut microbiome is significantly altered in inflammatory bowel diseases, but the basis of these changes is not well understood. We have combined metagenomic and metatranscriptomic profiling of the gut microbiome to assess changes to both bacterial community structure and transcriptional activity in a mouse model of colitis. Gene families involved in microbial resistance to oxidative stress, including Dps/ferritin, Fe-dependent peroxidase and glutathione S-transferase, were transcriptionally up-regulated in colitis, implicating a role for increased oxygen tension in gut microbiota modulation. Transcriptional profiling of the host gut tissue and host RNA in the gut lumen revealed a marked increase in the transcription of genes with an activated macrophage and granulocyte signature, suggesting the involvement of these cell types in influencing microbial gene expression. Down-regulation of host glycosylation genes further supports a role for inflammation-driven changes to the gut niche that may impact the microbiome. We propose that members of the bacterial community react to inflammation-associated increased oxygen tension by inducing genes involved in oxidative stress resistance. Furthermore, correlated transcriptional responses between host glycosylation and bacterial glycan utilisation support a role for altered usage of host-derived carbohydrates in colitis. Complementary transcription profiling data from the mouse hosts have also been deposited at ArrayExpress under accession number E-MTAB-3590 ( http://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-3590/ ).
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Project description:We combined an experimental microbiome of 11 bacterial strains isolated from the gut of native Caenorhabditis elegans. C. elegans were maintained on the experimental microbiome, Escherichia coli OP50 (control food source), or OP50 supplemented with cell-free media (CFM) from the experimental microbiome. For each of the three feeding conditions, RNA-seq was performed for wildtype (N2) worms or transgenic worms expressing amyloid beta 1-42 in their body wall muscle (GMC101).
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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:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
2020-11-30 | E-MTAB-8739 | biostudies-arrayexpress
Project description:The gut microbiome is significantly altered in inflammatory bowel diseases, but the basis of these changes is not well understood. We have combined metagenomic and metatranscriptomic profiling of the gut microbiome to assess changes to both bacterial community structure and transcriptional activity in a mouse model of colitis. Gene families involved in microbial resistance to oxidative stress, including Dps/ferritin, Fe-dependent peroxidase and glutathione S-transferase, were transcriptionally up-regulated in colitis, implicating a role for increased oxygen tension in gut microbiota modulation. Transcriptional profiling of the host gut tissue and host RNA in the gut lumen revealed a marked increase in the transcription of genes with an activated macrophage and granulocyte signature, suggesting the involvement of these cell types in influencing microbial gene expression. Down-regulation of host glycosylation genes further supports a role for inflammation-driven changes to the gut niche that may impact the microbiome. We propose that members of the bacterial community react to inflammation-associated increased oxygen tension by inducing genes involved in oxidative stress resistance. Furthermore, correlated transcriptional responses between host glycosylation and bacterial glycan utilisation support a role for altered usage of host-derived carbohydrates in colitis. Complementary RNA-seq and DNA-seq data sets of the microbiome from this study have also been deposited at ArrayExpress under accession number E-MTAB-3562 ( http://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-3562/ ).
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2023-02-24 | GSE225873 | GEO