Ontology highlight
ABSTRACT:
PROVIDER: PRJNA691429 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13415977_1.fastq.gz | Fastqsanger.gz | |||
| SRR13415977_2.fastq.gz | Fastqsanger.gz | |||
| SRR13415978_1.fastq.gz | Fastqsanger.gz | |||
| SRR13415978_2.fastq.gz | Fastqsanger.gz | |||
| SRR13415979_1.fastq.gz | Fastqsanger.gz |
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Project description:Opioids such as morphine have many beneficial properties as analgesics, however, opioids may induce multiple adverse gastrointestinal symptoms. We have recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. However, it is unclear how opioids modulate the gut homeostasis. By using a mouse model of morphine treatment, we studied effects of morphine treatment on gut microbiome. We characterized phylogenetic profiles of gut microbes, and found a significant shift in the gut microbiome and increase of pathogenic bacteria following morphine treatment when compared to placebo. In the present study, wild type mice (C57BL/6J) were implanted with placebo, morphine pellets subcutaneously. Fecal matter were taken for bacterial 16s rDNA sequencing analysis at day 3 post treatment. A scatter plot based on an unweighted UniFrac distance matrics obtained from the sequences at OTU level with 97% similarity showed a distinct clustering of the community composition between the morphine and placebo treated groups. By using the chao1 index to evaluate alpha diversity (that is diversity within a group) and using unweighted UniFrac distance to evaluate beta diversity (that is diversity between groups, comparing microbial community based on compositional structures), we found that morphine treatment results in a significant decrease in alpha diversity and shift in fecal microbiome at day 3 post treatment compared to placebo treatment. Taxonomical analysis showed that morphine treatment results in a significant increase of potential pathogenic bacteria. Our study shed light on effects of morphine on the gut microbiome, and its role in the gut homeostasis.
2018-04-16 | E-MTAB-5546 | biostudies-arrayexpress
Project description:Analysis of hematopoietic stem cells (HSC, Lineage-Sca-1+c-Kit+Flt3–CD34–). In order to better experiment, we treated mice with total body irradiation and local irradiation respectively. Next, the HSC were purified from the bone marrow of 8 weeks WT mice (Ctrl), total body radiation mice (IR), irradiated legs of locally irradiated mice (L_IR) and the other leg which unirradiated of locally irradiated mice (Ab_IR). Results provide the injury effect of IR on HSC under different conditions.
2024-06-05 | GSE244971 | GEO
Project description:The objective was to investigate the therapeutic effect of NeuroD on irradiation-induced intestinal injury at gene expression level. Gene expression profilings between NeuroD and EGFP treated mice which were received 9 Gy total body irradiation were compared.
2015-09-16 | GSE73068 | GEO
Project description:The objective was to investigate the therapeutic effect of VND3207 on irradiation-induced intestinal injury at gene expression level. Gene expression profilings between VND3207 and vehicle treated mice which were received 9 Gy total body irradiation were compared.
2016-10-18 | GSE88810 | GEO
Project description:Comparison of gene expression changes of FACS sorted splenic CD11b+CD8a- and CD11b-CD8a+ cDC subsets reconstituted in vivo following total body irradiation in combination with exogenous retinoic acid or vehicle control. Mice maintained on a control diet were subjected to 6 Gy total body irradiation and then provided exogenous retinoic acid or vehicle control beginning on D(+)3 after irradiation. All treated mice also received adoptive T cell transfer of either Trp-1 CD4+ or Pmel-1 CD8+ T cells, rVV, and IL-2. Splenic cDCs were isolated on D(+)10 after total body irradiation by FACS sorting.
2013-08-16 | E-GEOD-41021 | biostudies-arrayexpress
Project description:Purpose: To study the differential expression of gut bacterial mRNAs during chronic organophosphate treatment. Methods: Balb/c mice were treated with organophosphate (monocrotophos 28 ug/kg body weight/day) directly in drinking water for 180 days. Glucose tolerance tests indicated the induction of glucose intolerance. The total RNA was isolated by using TRIZOL from the cecal tissue that is cleared off fecal contents and subsequently the eukaryotic and bacterial rRNAs were removed by using MicrobExpress and MicrobEnrich kits (Ambion). Subsequently, RNA library was contructed using illumina kit as per manufacturer's instructions. Results: The reads were annotated to the reference human gut microbiome database and we found differential expression of large number of genes especially those involved in organophosphate degradation. Our subsequent studies proved that gut microbial degradation of organophosphates induces glucose intolerance via gluconeogenesis. Conclusions: Chronic organophosphate-induced hyperglycemia is mediated by the organosphosphate-degrading potential of gut microbiota.
2016-12-07 | GSE90843 | GEO
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:Sorted VE-Cadherin+ endothelial cells from C57/Bl6 mice at different time points following total body irradiation.
2019-12-11 | GSE141790 | GEO