Ontology highlight
ABSTRACT:
PROVIDER: PRJNA852600 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Use of MePS2-modified siRNAs to target GRAM Domain Containing 1B (GRAMD1B), a novel protein in taxane resistance. Two groups of samples are included: 1. siControl treated HeyA8-MDR and 2. siGRAMD1B treated HeyA8-MDR. Gene expression profiles of siGRAMD1B-HeyA8-MDR cells were compared to that of siControl-HeyA8MDR cells.
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Project description:Carbapenem-resistant Gram Negatives Genome sequencing and assembly
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Project description:Canadian Nosocomial Infection Surveillance Program on Carbapenemase Producing Gram-negatives
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Project description:Here, we report analysis of both the bacterial and host transcriptome as affected by colonization of R. hominis in the mouse gut. Microbial genes required for colonization and adaptation in the murine gut, as well as host genes responding to colonization by this bacterial species, were uncovered.
2016-02-05 | GSE25544 | GEO
Project description:Lactobacillus johnsonii, a Gram-positive, gut bacterium is well studied for its several health-beneficial properties. This
2024-07-15 | GSE271801 | GEO
Project description:RNA sequencing of Frischella perrara PEB0191 during in vitro growth and gut colonization
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Project description:Design: double blind controlled randomized trial with a parallel design and 3 treatment groups Description of subjects: Patients admitted in study centers for colorectal surgery under laporoscopy and/or laparotomy.
Product:
Product 1: BB536 and LA1 (10E9) Product 2: BB536 and LA1 (10E7) Placebo: Maltodextrin Number of patients: enrolled subjects: n=33, ITT data set: n=31, PP data set: n=30
Primary objective:
Colonization (biopsy+stools) of each bacteria for one of the dose at D0 (surgical procedure)
Secondary objectives:
* Influence of the probiotic bacteria on the gut microflora
* Modulation of the immune and inflammatory response
Additional objectives:
* Investigate dose effect on La1 colonization
* Investigate the effect of La1 colonization, treatment without La1 colonization, and absence of treatment and La1 colonization on other bacteria and on immunological parameters
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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.
2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress
Project description:Gut-microbiota membership is associated with diverse neuropsychological-diseases, including substance use disorders (SUDs). Unravelling mechanistic interactions between gut microbes and the host during psychostimulant use remains challenging. Here we show that cocaine exposure increases intestinal levels of norepinephrine, sensed through the bacterial adrenergic receptor QseC, promoting intestinal colonization of g-Proteobacteria. Gut colonization by g-Proteobacteria depletes the neuroactive metabolite glycine (used as a nitrogen source) both in the gut and cerebrospinal fluid, enhancing host cocaine-induced behaviors. Glycine repletion reversed this response, and intestinal colonization by g-Proteobacteria unable to uptake glycine did not alter the host response to cocaine. Transcriptomic profiling indicates a role of g-Proteobacteria modulated glycine levels in cocaine induced transcriptional plasticity in the nucleus accumbens through the glutamatergic transmission. Altogether, we introduce a mechanism by which intestinal bacteria alter the host’s brain responses to cocaine that could be exploited to modulate reward-related brain circuits that contribute to SUDs.
2022-09-07 | GSE212421 | GEO