Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1146721 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30202083_1.fastq.gz | Fastqsanger.gz | |||
| SRR30202083_2.fastq.gz | Fastqsanger.gz | |||
| SRR30202084_1.fastq.gz | Fastqsanger.gz | |||
| SRR30202084_2.fastq.gz | Fastqsanger.gz | |||
| SRR30202085_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose：We used transcriptome sequencing to study the mechanism of sugar and lipid excesses on nematode growth and development. Methods：Nematodes grew to L4 phase and collected nematodes from different treatment groups, including control group without any treatment, 400 mM sucrose, 500 ug/ml stearic acid, co-treatment with sucrose and stearic acid, and co-treatment with resveratrol-sucrose-stearic acid, 3 replicates per group. Extract total RNA, detect RNA quality, library preparation, sequencing, and analyze data Results:Reads were obtained for each sample using Illumina Hiseq X Ten sequencing. After discarding the low-quality reads, corresponding to 48 million clean reads obtained from sequencing were mapped on the reference genome of C. elegans (GCF_000002985.6). High Pearson's correlation coefficients of FPKM distribution between the three biological replicates for each sample were detected (R2 = 0.93-0.99, P < 0.001) , reflecting the robustness of our library preparation from nematodes’ RNA samples.Compared with control group, there were 905 DEGs in the sucrose group , of which 387 genes were upregulated and 518 genes were downregulated. Similarly, there were 698 DEGs in the stearic acid group , including 367 upregulated and 331 downregulated DEGs. Compared with control group, there were 1014 DEGs in group SUC-STE, including 476 upregulated DEGs, and 538 downregulated DEGs. Moreover, in contrast to the sucrose-stearic acid group, there were 10 DEGs after treated with resveratrol, including 5 upregulated DEGs and 5 downregulated DEGs.
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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:Chronic acid suppression by proton pump inhibitor (PPI) has been hypothesized to alter the gut microbiota via a change in intestinal pH. To evaluate the changes in gut microbiota composition by long-term PPI treatment. Twenty-four week old F344 rats were fed with (n = 5) or without (n = 6) lansoprazole (PPI) for 50 weeks. Then, profiles of luminal microbiota in the terminal ileum were analyzed. Pyrosequencing for 16S rRNA gene was performed by genome sequencer FLX (454 Life Sciences/Roche) and analyzed by metagenomic bioinformatics.
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Project description:Plant damage promotes the interaction of lipoxygenases (LOX) with fatty acids yielding 9-hydroperoxides, 13-hydroperoxides and complex arrays of oxylipins. The action of 13-LOX on linolenic acid enables production of 12-oxo-phytodienoic acid (12-OPDA) and its downstream products, termed jasmonates. As signals, jasmonates have related yet distinct roles in the regulation of plant resistance against insect and pathogen attack. A similar pathway involving 9-LOX activity on linolenic and linoleic acid leads to the 12-OPDA positional isomer, 10-oxo-11-phytodienoic acid (10-OPDA) and 10-oxo-11-phytoenoic acid (10-OPEA), respectively; however, physiological roles for 9-LOX cyclopentenones have remained unclear. In developing maize (Zea mays) leaves, southern leaf blight (Cochliobolus heterostrophus) infection results in dying necrotic tissue and the localized accumulation of 10-OPEA, 10-OPDA and a series of related 14- and 12-carbon metabolites, collectively termed ‘death acids’. 10-OPEA accumulation becomes wound-inducible within fungal-infected tissues and at physiologically relevant concentrations acts as a phytoalexin by suppressing the growth of fungi and herbivores including Aspergillus flavus, Fusarium verticillioides, and Helicoverpa zea. Unlike previously established maize phytoalexins, 10-OPEA and 10-OPDA display significant phytotoxicity. Both 12-OPDA and 10-OPEA promote the transcription of defense genes encoding glutathione S-transferases, cytochrome P450s, and pathogenesis-related proteins. In contrast, 10-OPEA only weakly promotes the accumulation of multiple protease inhibitor transcripts. Consistent with a role in dying tissue, 10-OPEA application promotes cysteine protease activation and cell death which is inhibited by overexpression of the cysteine protease inhibitor maize cystatin-9. Functions for 10-OPEA and associated death acids are consistent with specialized roles in local defense reactions.
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Project description:Plant cellular damage promotes the interaction of lipoxygenases (LOX) with free fatty acids to yield 9- and 13-hydroperoxides which are further metabolized into diverse oxylipins. The enzymatic action of 13-LOX on linolenic acid enables production of 12-oxo-phytodienoic acid (12-OPDA) and its downstream products, jointly known as jasmonates. As signals, jasmonates have related yet distinct roles in the regulation of plant resistance against insect and pathogen attack. An additional and conceptually parallel pathway involving 9-LOX activity on linoleic acid leads to the production of 10-oxo-11-phytoenoic acid (10-OPEA). Despite structural similarity to jasmonates, physiological roles for 10-OPEA have remained unclear. Both 12-OPDA and 10-OPEA equally promote the transcription of numerous defense genes encoding glutathione S-transferases, cytochrome P450s, and pathogenesis-related proteins; however, 10-OPEA activity diverges in the context of reduced protease inhibitor transcript accumulation. To identify additional differential responses, we subsequently performed whole transcriptome analyses using RNAseq. These comparisons provide a platform for further examination of plant response specificity to the cyclopentenone 10-OPEA.
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