Ontology highlight
ABSTRACT:
PROVIDER: PRJNA872502 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21177300_1.fastq.gz | Fastqsanger.gz | |||
| SRR21177300_2.fastq.gz | Fastqsanger.gz | |||
| SRR21177400_1.fastq.gz | Fastqsanger.gz | |||
| SRR21177400_2.fastq.gz | Fastqsanger.gz | |||
| SRR21177500_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: Idiopathic Chronic Diarrhea (ICD) is a common cause of morbidity and mortality among juvenile rhesus macaques. Characterized by chronic inflammation of the colon and repeated bouts of diarrhea, ICD is largely unresponsive to medical interventions including corticosteroid, antiparasitic and antibiotic treatments. Although ICD is accompanied by large disruptions in the composition of the commensal gut microbiome, no single pathogen has been concretely identified as responsible for the onset and continuation of the disease. Results: Fecal samples were collected from twelve ICD-diagnosed macaques and twelve age and sex-matched controls. RNA was extracted for metatranscriptomic analysis of species and activity within the gut microbiome. Using SAMSA2, these samples were contrasted to identify shifts both in overall organism activity and functional activity. Bacterial, fungal, archaeal, protozoan, and macaque (host) transcripts were simultaneously assessed. ICD-afflicted animals were characterized by increased activity of known bacterial pathogens and by decreased activity of archaeal methanogens. Interestingly, known fungal opportunists were not increased in ICD, nor were the usual enteric protozoans, although Trichomonas activity is up-regualted. Known mucin degrading organisms and mucin-degrading enzymes were up-regulated in the fecal microbiomes of ICD-afflicted animals. Assessment of colon sections using immunohistochemistry confirmed differential mucin composition between healthy control and ICD animals. Finally, assessment of host-derived transcripts confirms colonic inflammation and suggests that the lumen is infiltrated by granulocytes. Conclusions: The simultaneous profiling of bacterial, fungal, archaeal, protozoan, and macaque transcripts from stool samples suggests that ICD of rhesus macaques is associated with increased pathogen activity and altered mucin degradation.
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Project description:Deep sequencing of small RNA from three closely related brassicaceae A. thaliana, A. lyrata and Capsella rubella was done to systematically analyze the evolution of MIRNA genes and their targets. Small RNA were extracted from total RNA by size fractionation and converted to DNA amplicons by serial adaptor ligation to both ends followed by RT-PCR. DNA amplicons were sequenced using an Ilumina Genome Analyzer. Resulting sequences were computationally trimmed to remove 3' adaptor sequences. Raw data files (fastq) are unavailable for two of the samples (A.lyrata_flowers-stage1-12_rep1 and A.lyrata_flowers-stage1-12_rep2).
2010-05-14 | E-GEOD-20660 | biostudies-arrayexpress
Project description:Rationale: Recent studies suggest a potential link between gut bacterial microbiota dysbiosis and PAH, but the exact role of gut microbial communities, including bacteria, archaea, and fungi, in PAH remains unclear. Objectives: To investigate the role of gut microbiota dysbiosis in idiopathic pulmonary arterial hypertension (IPAH) and to assess the therapeutic potential of fecal microbiota transplantation (FMT) in modulating PAH progression. Methods: Using shotgun metagenomics, we analyzed gut microbial communities in IPAH patients and healthy controls. FMT was performed to transfer gut microbiota from IPAH patients or MCT-PAH rats to normal rats and from healthy rats to MCT-PAH rats. Hemodynamic measurements, echocardiography, histological examination, metabolomic and RNA-seq analysis were conducted to evaluate the effects of FMT on PAH phenotypes. Measurements and Main Results: Gut microbiota analysis revealed significant alterations in the bacterial, archaeal, and fungal communities in IPAH patients compared to healthy controls. FMT from IPAH patients induced PAH phenotypes in recipient rats. Conversely, FMT from healthy rats to IPAH rats significantly ameliorated PAH symptoms, restored gut microbiota composition, and normalized serum metabolite profiles. Specific microbial species were identified with high diagnostic potential for IPAH, improving predictive performance beyond individual or combined microbial communities. Conclusions: This study establishes a causal link between gut microbiota dysbiosis and IPAH and demonstrates the therapeutic potential of FMT in reversing PAH phenotypes. The findings highlight the critical role of bacterial, archaeal, and fungal communities in PAH pathogenesis and suggest that modulation of the gut microbiome could be a promising treatment strategy for PAH.
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