Human metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA46339 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR404998.fastq.gz | Fastqsanger.gz | |||
| SRR404999.fastq.gz | Fastqsanger.gz | |||
| SRR405000.fastq.gz | Fastqsanger.gz | |||
| SRR405001.fastq.gz | Fastqsanger.gz |
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Project description:<p>This project explores the nature of the human intestinal microbiome in healthy children and children with recurrent abdominal pain. The overall goal is to obtain a robust knowledge-base of the intestinal microbiome in children without evidence of pain or gastrointestinal disease, children with functional abdominal pain, and children with abdominal pain and changes in bowel habits (irritable bowel syndrome). Multiple strategies have been deployed to navigate and understand the nature of the intestinal microbiome in childhood. These strategies include 454 pyrosequencing-based strategies to sequence 16S rRNA genes and understand the detailed composition of microbes in healthy and disease groups. Microarray-based hybridization with the PhyloChip and quantitative real-time PCR (qPCR) probes are being applied as complementary strategies to gain an understanding of the intestinal microbiome from various perspectives. Data collected and analyzed during the HMP UH2 and UH3 Demo project, from a set of healthy and IBS children may enable the identification of core microbiomes in children in addition to variable components that may distinguish healthy from diseased pediatric states. We are currently analyzing the dataset for the presence of disease-specific signatures in the human microbiome, and correlating these microbial signatures with pediatric health or IBS disease status. This study explores the nature of core and variable human microbiomes in pre-adolescent healthy children and children with recurrent abdominal pain.</p>
| phs000265.v3.p1 | EGA
Project description:<p>This project explores the nature of the human intestinal microbiome in healthy children and children with recurrent abdominal pain. The overall goal is to obtain a robust knowledge-base of the intestinal microbiome in children without evidence of pain or gastrointestinal disease, children with functional abdominal pain, and children with abdominal pain and changes in bowel habits (irritable bowel syndrome). Multiple strategies have been deployed to navigate and understand the nature of the intestinal microbiome in childhood. These strategies include 454 pyrosequencing-based strategies to sequence 16S rRNA genes and understand the detailed composition of microbes in healthy and disease groups. Microarray-based hybridization with the PhyloChip and quantitative real-time PCR (qPCR) probes are being applied as complementary strategies to gain an understanding of the intestinal microbiome from various perspectives. Data collected and analyzed during the HMP UH2 and UH3 Demo project, from a set of healthy and IBS children may enable the identification of core microbiomes in children in addition to variable components that may distinguish healthy from diseased pediatric states. We are currently analyzing the dataset for the presence of disease-specific signatures in the human microbiome, and correlating these microbial signatures with pediatric health or IBS disease status. This study explores the nature of core and variable human microbiomes in pre-adolescent healthy children and children with recurrent abdominal pain.</p>
| phs000265 | dbGaP
Project description:Gene expression profiling of pediatric patients with simple appendicitis (SA) compared to perforated appendicitis (PA) and non-appendicitis abdominal pain (NAAP).
2024-02-20 | GSE225466 | GEO
Project description:We studied 64 patients admitted to the Florence main hospital emergency room with severe abdominal pain. A blood sample was drawn from each patient at admission, and the corresponding sera underwent 1H NMR metabolomics fingerprinting. Unsupervised PCA analysis showed a significant discrimination between a group of patients with symptoms of upper abdominal pain and a second group consisting of patients with diffuse abdominal/intestinal pain. Prompted by this observation, supervised statistical analysis (OPLS-DA) showed a very good discrimination (> 90 %) between the two groups of symptoms. Actually in the present study, upper abdominal pain may result from either symptomatic gallstones, cholecystitis or pancreatitis, while diffuse abdominal/intestinal pain may result from either intestinal ischemia, strangulated obstruction or mechanical obstruction. Although limited by the small number of samples from each of these six conditions, discrimination of these diseases was attempted. In the first symptom group, > 70% discrimination accuracy was obtained among symptomatic gallstones, pancreatitis and cholecystitis, while for the second symptom group > 85% classification accuracy was obtained for intestinal ischemia, strangulated obstruction and mechanical obstruction. No single metabolite stands up as a possible biomarker for any of these diseases, while the contribution of the whole 1H NMR serum fingerprint seems to be a promising candidate, to be confirmed on larger cohorts, as a first-line discriminator for these diseases.
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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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