Ontology highlight
ABSTRACT:
PROVIDER: PRJNA731317 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14605303_1.fastq.gz | Fastqsanger.gz | |||
| SRR14605303_2.fastq.gz | Fastqsanger.gz | |||
| SRR14605304_1.fastq.gz | Fastqsanger.gz | |||
| SRR14605304_2.fastq.gz | Fastqsanger.gz | |||
| SRR14605305_1.fastq.gz | Fastqsanger.gz |
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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
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:Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a life-threatening condition characterized by lung inflammation and damage. Mechanical ventilation can exacerbate this condition. The gut microbiome, known to impact health, might have implications for ALI/ARDS outcomes. This study aimed to investigate the effects of probiotics in a murine ALI model. Using a two-hit approach combining lipopolysaccharide-induced inflammation and mechanical ventilation-induced injury, a severe lung injury model was established in mice. Probiotics containing Bifidobacterium spp. were administered due to their known interactions with immune cells and immune pathway modulation. The effects of probiotic administration on lung inflammation severity were evalu ated through biochemical, and histological analyses of lung tissue, and single-cell RNA sequencing analysis. Probiotic administration increased Bifidobacterium spp. composition in the gut microbiota and mitigated lung damage and inflammation. Single-cell RNA sequencing revealed the stimulation of Anxa1high macrophages, possibly promoting anti-inflammatory responses.
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Project description:Transcriptional profiling of mouse gut wall tissue following infection with Salmonella or treatment with Probiotics to see the role of probiotics in preventing salmonella infection through gut mucosal route of mouse.
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Project description:Recent evidence has demonstrated that the gut microbiome has marked effects on neuronal function and behavior. Disturbances to microbial populations within the gut have been linked to myriad models of neuropsychiatric disorders. However, the role of the microbiome in substance use disorders remains understudied. Here we show that male mice with their gut microbiome depleted by nonabsorbable antibiotics (Abx) exhibit decreased formation of morphine conditioned place preference across a range of doses (2.5-15 mg/kg), have decreased locomotor sensitization to morphine, and demonstrate marked changes in gene expression within the nucleus accumbens (NAc) in response to high-dose morphine (20 mg/kg × 7 days). Replacement of short-chain fatty acid (SCFA) metabolites, which are reduced by microbiome knockdown, reversed the behavioral and transcriptional effects of microbiome depletion. This identifies SCFA as the crucial mediators of microbiome-brain communication responsible for the effects on morphine reward caused by microbiome knockdown. These studies add important new behavioral, molecular, and mechanistic insight to the role of gut-brain signaling in substance use disorders
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