Ontology highlight
ABSTRACT:
PROVIDER: PRJNA802995 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17868201_1.fastq.gz | Fastqsanger.gz | |||
| SRR17868201_2.fastq.gz | Fastqsanger.gz | |||
| SRR17868202_1.fastq.gz | Fastqsanger.gz | |||
| SRR17868202_2.fastq.gz | Fastqsanger.gz | |||
| SRR17868203_1.fastq.gz | Fastqsanger.gz |
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Project description:Piscirickettsiosis or salmonid rickettsial septicemia (SRS) caused by intracellular Gram-negative bacterial pathogen, Piscirickettsia salmonis, constitutes one of the main infectious diseases in salmonid aquaculture. In the present study, we aimed to explore the transcriptomic responses in the Atlantic salmon kidney following a low dose of EM-90-like P. salmonis infection using the consortium for Genomic Research on All Salmonids Project (cGRASP)-designed Agilent 44K salmonid oligonucleotide microarray. Two infection level phenotypes [low (L-SRS) and high (H-SRS) infection level] were revealed in infected individuals at 21 days post-injection (DPI) based on multivariate analyses of expression of four antibacterial biomarker transcripts (campb, hampa, il8a, tlr5a) and pathogen level measured by qPCR. Five fish from each group (Control, L-SRS, and H-SRS) were selected for transcriptome profiling. We identified 1636 and 3076 differentially expressed probes (DEPs) in the L-SRS and H-SRS groups, respectively (FDR = 0.01).
2021-12-13 | GSE178327 | GEO
Project description:The gut epithelium exhibits regional specialization critical for its function and susceptibility to disease, as gut diseases localize to specific regions of the organ. However, how regionalization is established and its influence on disease susceptibility remain poorly understood. Here, we investigate the role of the gut microbiome—which comprises all microorganisms residing in the gut lumen and is itself regionalized—in regulating regionalization of the colon. We demonstrate that the regional identity of colonocytes is disrupted in mice lacking a microbiome. Mechanistically, we show that the proximal colonic microbiome produces high levels of nicotinic acid, which induces Pparα expression to establish proximal colonocyte identity. Furthermore, we find that microbiome-driven proximal identity confers protection against tissue injury in the mouse. Finally, we show that colon regionalization and the loss of proximal identity during disease are also present in human.
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Project description:The gut epithelium exhibits regional specialization critical for its function and susceptibility to disease, as gut diseases localize to specific regions of the organ. However, how regionalization is established and its influence on disease susceptibility remain poorly understood. Here, we investigate the role of the gut microbiome—which comprises all microorganisms residing in the gut lumen and is itself regionalized—in regulating regionalization of the colon. We demonstrate that the regional identity of colonocytes is disrupted in mice lacking a microbiome. Mechanistically, we show that the proximal colonic microbiome produces high levels of nicotinic acid, which induces Pparα expression to establish proximal colonocyte identity. Furthermore, we find that microbiome-driven proximal identity confers protection against tissue injury in the mouse. Finally, we show that colon regionalization and the loss of proximal identity during disease are also present in human.
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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:Stereotactic radiosurgery (SRS) has been shown to be efficacious for treatment of limited brain metastasis (BM), however, the effects of SRS on human brain metastases have yet to be studied. We performed genomic analysis of resected brain metastases from patients whose resected lesion was previously treated with SRS. Our analyses demonstrated for the first time that patients possess a distinct genomic signature based on type of treatment failure including local failure, leptomeningeal spread, and radio-necrosis. Examination of the center and peripheral edge of the tumors treated with SRS indicated differential DNA damage distribution and an enrichment for tumor suppressor mutations and DNA damage repair pathways along the peripheral edge. Furthermore, the two clinical modalities used to deliver SRS, LINAC and GK, demonstrated differential effects on the tumor landscape even between controlled primary sites. Our study provides, in humans, biological evidence of differential effects of SRS across BM’s.
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Project description:Stereotactic radiosurgery (SRS) has been shown to be efficacious for treatment of limited brain metastasis (BM), however, the effects of SRS on human brain metastases have yet to be studied. We performed genomic analysis of resected brain metastases from patients whose resected lesion was previously treated with SRS. Our analyses demonstrated for the first time that patients possess a distinct genomic signature based on type of treatment failure including local failure, leptomeningeal spread, and radio-necrosis. Examination of the center and peripheral edge of the tumors treated with SRS indicated differential DNA damage distribution and an enrichment for tumor suppressor mutations and DNA damage repair pathways along the peripheral edge. Furthermore, the two clinical modalities used to deliver SRS, LINAC and GK, demonstrated differential effects on the tumor landscape even between controlled primary sites. Our study provides, in humans, biological evidence of differential effects of SRS across BM’s.
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Project description:Function-damaging variants in the TRIO gene are enriched in individuals with neurodevelopmental disorders (NDDs). TRIO encodes a cytoskeletal regulatory protein with three catalytic domains – two guanine exchange factor (GEF) domains, GEF1 and GEF2, and a kinase domain, as well as several accessory domains that have not been extensively studied. Disease variants in the GEF1 domain or the nine adjacent spectrin repeats (SRs) are enriched in NDDs, suggesting that dysregulated GEF1 activity is linked to these disorders. We provide evidence here that the Trio SRs interact intramolecularly with the GEF1 domain to inhibit its activity. We demonstrate that SRs 6-9 decrease GEF1 catalytic activity both in vitro and in cells and show that NDD-associated variants in the SR8 and GEF1 domains relieve this autoinhibitory constraint. Our results from chemical cross-linking and BioLayer Interferometry indicate that the SRs primarily contact the PH region of the GEF1 domain, reducing GEF1 binding to Rac1. Together, our findings reveal a key regulatory mechanism that is commonly disrupted in multiple NDDs and may offer a new target for therapeutic intervention for TRIO-associated NDDs.
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