Donor mice gut microbiome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1136793 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29908722.fastq.gz | Fastqsanger.gz | |||
| SRR29908723.fastq.gz | Fastqsanger.gz | |||
| SRR29908724.fastq.gz | Fastqsanger.gz | |||
| SRR29908725.fastq.gz | Fastqsanger.gz | |||
| SRR29908726.fastq.gz | Fastqsanger.gz |
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Project description:We used microarrays to investigate gene expression changes in leukemic cells from Pax5+/- mice treated with antibiotics. Precursor B cell acute lymphoblastic leukemia (pB-ALL), the most common type of childhood leukemia, is frequently characterized by the cooperation of a genetic predisposition acquired in utero and secondary oncogenic events taking place only in a fraction of predisposed children after birth. Although predisposition can be detected at birth, it is currently unknown which factors determine the development of overt leukemia in genetic carriers and how this can be potentially prevented. Experimental studies have shown that infectious stimuli promote disease onset in genetically predisposed mice. Here, we analyzed the impact of the microbiome on leukemogenesis in a mouse model (Pax5+/- mice) that faithfully mimicks genetic predisposition and leukemogenesis of human pB-ALL related to the synergy of genetic predisposition and exposure to a natural infectious environment. Employing 16S rRNA sequencing and machine learning we can accurately predict a distinct gut microbiome which is determined by a specific constitutional genetic variant. Deprivation of the gut microbiome by antibiotic treatment enhanced pB-ALL development in Pax5+/- predisposed (63% vs. 22%) but not in wildtype mice (0%). This finding was observed in the presence but also -to a lesser extent- in the absence of a natural, infectious environment (48%). The composition of the gut microbiome constitutes a biomarker signature and allows to identify specifically those Pax5+/- mice that developed leukemia. This indicates that the gut microbiome can be used to identify carriers at risk to develop leukemia and to reduce this risk by early-life interventions.
2019-10-30 | GSE139547 | GEO
Project description:Opioid analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit long term use. In the current study using a chronic morphine-murine model a longitudinal approach was undertaken to investigate the role of morphine modulation of gut microbiome as a mechanism contributing to the negative consequences associated with opioids use. The results revealed a significant shift in the gut microbiome and metabolome within 24 hours following morphine treatment when compared to placebo. Morphine induced gut microbial dysbiosis exhibited distinct characteristic signatures profiles including significant increase in communities associated with pathogenic function, decrease in communities associated with stress tolerance. Collectively, these results reveal opioids-induced distinct alteration of gut microbiome, may contribute to opioids-induced pathogenesis. Therapeutics directed at these targets may prolong the efficacy long term opioid use with fewer side effects.
2018-04-16 | E-MTAB-5550 | biostudies-arrayexpress
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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.
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Project description:Abstract: Many mouse models of neurological disease use the tetracycline transactivator (tTA) system to control transgene expression by oral treatment with the broad-spectrum antibiotic doxycycline. Antibiotic treatment used for transgene control might have undesirable systemic effects, including the potential to affect immune responses in the brain via changes in the gut microbiome. Recent work has shown that an antibiotic cocktail to perturb the gut microbiome can suppress microglial reactivity to brain amyloidosis in transgenic mouse models of Alzheimer's disease based on controlled overexpression of the amyloid precursor protein (APP). Here we assessed the impact of chronic low dose doxycycline on gut microbiome diversity and neuroimmune response to systemic LPS challenge in a tTA-regulated model of Alzheimer's amyloidosis. We show that doxycycline decreased microbiome diversity in both APP transgenic and wild-type mice and that these changes persisted long after drug withdrawal. Despite this change in microbiome composition, dox treatment had minimal effect on transcriptional signatures in the brain, both at baseline and following acute LPS challenge. Our findings suggest that central neuroinflammatory responses may be less affected by dox at doses needed for transgene control than by antibiotic cocktail at doses used for microbiome manipulation.
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