Ontology highlight
ABSTRACT:
PROVIDER: PRJNA773235 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16556011_1.fastq.gz | Fastqsanger.gz | |||
| SRR16556011_2.fastq.gz | Fastqsanger.gz | |||
| SRR16556012_1.fastq.gz | Fastqsanger.gz | |||
| SRR16556012_2.fastq.gz | Fastqsanger.gz | |||
| SRR16556013_1.fastq.gz | Fastqsanger.gz |
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Project description:The pathogenesis of primary sclerosing cholangitis (PSC) is unclear, although studies implicate IL-17A as an inflammatory mediator in this disease. However, a direct assessment of IL-17 signaling in PSC cholangiocytes is lacking. Cholangiocytes obtained from PSC and non-PSC patients by endoscopic retrograde cholangiography (ERC) were cultured as extrahepatic cholangiocyte organoids (ECO). The ECO were treated with vehicle or IL-17A and assessed by NanoString analysis, single cell RNA sequencing (scRNA-seq), and whole genome sequencing (WGS). The secretome was assessed by Olink analysis. Unsupervised clustering of all integrated scRNA-seq data identified 8 cholangiocyte clusters which did not differ between non-PSC and PSC ECO. However, PSC ECO cells demonstrated a much more robust response to IL-17 treatment, noted by an increased number of differentially expressed genes (DEG) after the treatment with IL-17A, compared to non-PSC ECO. After rigorous filtering, WGS identified the presence of somatic mutations that were shared between PSC ECO. However, no somatic mutations dysregulating genes in the IL-17 pathway were identified. The secretome of PSC ECO contained more abundant chemokines and cytokines under basal conditions and following IL-17A stimulation when compared to non-PSC ECO. In conclusion, PSC and non-PSC patient derived ECO respond differently to IL-17 stimulation regardless of mutational status, suggesting a change in epigenetic regulation and the implication of this pathway in the pathogenesis of PSC.
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Project description:Currently, the only sustainable alternatives for dietary fish oil (FO) in aquafeeds are vegetable oils (VO) that are devoid of omega-3 (n-3) long-chain polyunsaturated fatty acids (LC-PUFA). Entirely new sources of n-3 LC-PUFA such as eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids through de novo production is a potential solution to fill the gap between supply and demand of these important nutrients. Camelina sativa,was metabolically engineered to produce a seed oil (ECO) with > 20 % EPA and its potential to substitute for FO in Atlantic salmon feeds was tested. Fish were fed one of three experimental diets containing FO, wild-type camelina oil (WCO) or ECO as the sole lipid sources for 7-weeks. Inclusion of ECO did not affect any of the performance parameters studied and enhanced apparent digestibility of individual n-6 and n-3 PUFA compared to dietary WCO. High levels of EPA were maintained in brain, liver and intestine (pyloric caeca), and levels of DPA and DHA were increased in liver and intestine of fish fed ECO compared to fish fed WCO likely due to increased LC-PUFA biosynthesis based on up-regulation of the genes. Fish fed WCO and ECO showed slight lipid accumulation within hepatocytes similar to that with WCO, although not significantly different to fish fed FO. The regulation of a small number of genes could be attributed to the specific effect of ECO (311 features) with metabolism being the most affected category. The EPA oil from transgenic Camelina (ECO) could be used as a substitute for FO, however it is a hybrid oil containing both FO (EPA) and VO (18:2n-6) fatty acid signatures that resulted in similarly mixed metabolic and physiological responses.
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