Ontology highlight
ABSTRACT:
PROVIDER: PRJNA766833 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Human gut microbiota preservation for functional studies: in-vitro comparison of common cryoprotective agents
| PRJNA310059 | ENA
Project description:Fecal Microbiota rawdata from autistic model mice. Female and Male Poly I:C treated mice were compared at microbiota level.
2023-05-04 | E-MTAB-11150 | biostudies-arrayexpress
Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed cohousing experiments to test if Paneth cell phenotype is horizontally transmissible as is microbiota. Atg16l1 T300A and littermate controls that were exposed to cigarette smoking were used as microbiota donors, and these donor mice were exposed to smoking for 2 weeks prior to cohousing. Separate groups of Atg16l1 T300A and littermate controls that were not exposed to cigarette smoking were used as microbiota recipients. The microbiota recipients were co-housed with microbiota donors of the same genotype for 4 weeks, during this period the donors continued to be exposed to cigarette smoking. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. At the end of the experiment, the fecal microbiota composition was analyzed by 16S rRNA sequencing.
2018-10-31 | E-MTAB-5720 | biostudies-arrayexpress
Project description:Study of preservation conditions on viability of human stool microbiota
| PRJNA634503 | ENA
Project description:We profiled transcriptome and accessible chromatin landscapes in intestinal epithelial cells (IECs) from mice reared in the presence or absence of microbiota. We show that regional differences in gene transcription along the intestinal tract were accompanied by major alterations in chromatin organization. Surprisingly, we discovered that microbiota modify host gene transcription in IECs without significantly impacting the accessible chromatin landscape. Instead, microbiota regulation of host gene transcription might be achieved by differential expression of specific TFs and enrichment of their binding sites in nucleosome depleted CRRs near target genes. Our results suggest that the chromatin landscape in IECs is pre-programmed by the host in a region-specific manner to permit responses to microbiota through binding of open CRRs by specific TFs. mRNA and accessible chromatin (DNase-seq) profiles from colonic and ileal IECs were compared between conventionally-raised (CR), germ-free (GF), and conventionalized (CV) C57BL/6 mice.
2014-06-07 | E-GEOD-57919 | biostudies-arrayexpress
Project description:In vitro gut microbiota models are often used to study drug-microbiome interaction. Similar to culturing individual microbial strains, the biomass accumulation of in vitro gut microbiota follows a logistic growth curve. Current studies on in vitro gut microbiome responses introduce drug stimulation during different growth stages, e.g. lag phase or stationary phase. However, in vitro gut microbiota in different growth phases may respond differently to a same stimuli. Therefore, in this study, we used a 96-deep well plate-based culturing model (MiPro) to culture the human gut microbiota. Metformin, as the stimulus, was added at the lag, log and stationary phases of growth. Microbiome samples were collected at different time points for optical density and metaproteomic functional analysis. Results show that in vitro gut microbiota responded differently to metformin added during different growth phases, in terms of the growth curve, alterations of taxonomic and functional compositions. The addition of drugs at log phase leads to the greatest decline of bacterial growth. Metaproteomic analysis suggested that the strength of the metformin effect on the gut microbiome functional profile was ranked as lag phase > log phase > stationary phase. Our results showed that metformin added at lag phase resulted in a significantly reduced abundance of the Clostridiales order as well as an increased abundance of the Bacteroides genus, which was different from stimulation during the rest of the growth phase. Metformin also resulted in alterations of several pathways, including energy production and conversion, lipid transport and metabolism, translation, ribosomal structure and biogenesis. Our results indicate that the timing for drug stimulation should be considered when studying drug-microbiome interactions in vitro.
2022-03-01 | PXD017390 | Pride
Project description:The aim of this study was to develop a suitable method to preserve fecal samples for metaproteomics analyses when flash-freezing is not an option. Fecal samples were collected from conventional adult C57BL/6 mice and combined into a fecal master mix. The fecal master mix was then split into 48 subsamples that were subjected to different preservation treatments. The following six preservation methods were tested: flash-freezing in liquid nitrogen followed by storage at -80°C, immersion in RNAlater® and storage at room temperature, immersion in RNAlater® and immediate storage at -80°C, immersion in 95% ethanol and storage at room temperature, immersion in a RNAlater-like buffer “NAP buffer” and storage at room temperature, and immersion in an autoclaved RNAlater-like buffer “Autoclaved NAP buffer” and storage at room temperature. Proteins were extracted from the samples after being stored for 1 and 4 weeks. There were 4 replicates per treatment and time-point. Samples were analyzed by LC-MS/MS and the data were analyzed with Proteome Discoverer against a large database of mouse microbiota protein sequences.
2021-11-25 | PXD024115 | Pride
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