Mouse gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB14660 | ENA |
REPOSITORIES: ENA
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Project description:The intestinal microbiota modulates host physiology and gene expression via mechanisms that are not fully understood. A recently discovered layer of gene expression regulation is N6-methyladenosine (m6A) and N6,2′ -O-dimethyladenosine (m6Am) modifications of mRNA. To unveil if these epitranscriptomic marks are affected by the gut microbiota, we performed methylated RNA-immunoprecipitation and sequencing (MeRIP-seq) to examine m6A-modifications in transcripts of mice displaying either a conventional, or a modified, or no gut microbiota and discovered that the microbiota has a strong influence on m6A- modifications in the cecum, and also, albeit to a lesser extent, in the liver, affecting pathways related to metabolism, inflammatory and antimicrobial responses . We furthermore analysed expression levels of several known writer and eraser enzymes and found the methyltransferase Mettl16 to be downregulated in absence of a microbiota. As a consequence, one of its targets, the S-adenosyl methionine synthase Mat2a was less expressed in mice without gut flora. We furthermore show that distinct commensal bacteria, Akkermansia muciniphila, Lactobacillus plantarum can affect specific m6A modifications. Together, we report here epitranscriptomic modifications as an additional level of interaction in the complex interplay between commensal bacteria and their host.
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Project description:Constant availability of food can contribute to the pathogenesis of metabolic syndrome and type 2 diabetes. Short term intermittent fasting (IF) can reset the central, light-entrained (suprachiastmatic nucleus) clock and also the peripheral, food-entrained (liver) clock to restore metabolic homeostasis in T2D. We asked if long term IF could prevent development of diabetic retinopathy (DR) in a type 2 diabetes model, the db/db mouse. After 7 months, IF corrected diabetes-induced increases in triglycerides, cholesteryl esters and diglycerides. IF protocol in db/db mice also prevented development of DR. In addition, host frequency and time of food intake affected the gut microbiome composition. IF led to decreased levels of Clostridiales and Akkermansia muciniphila in db/db mice and these changes in flora were accompanied by increased gut mucin, goblet cell number and villus length. Increased levels of Firmicutes in db/db mice on IF supported improved bile acid metabolism. To confirm that the restoration of bile acid function could contribute to the beneficial effects induced by IF on DR, the dual FXR/TGR-5 agonist INT-767 was administered to a second diabetes model, DBA2J mice injected with streptozotocin (STZ) and placed on Western diet (WD). In this model, INT-767 prevented development of DR. These findings support the concept that long-term IF mediates multiple beneficial effect by restoring the gut-liver axis homeostasis.
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Project description:Accidental or iatrogenic ionizing radiation exposure precipitates acute and chronic radiation injuries. Traditional paradigm of mitigating radiotherapy-associated side effects has ignored the gender-specific dimorphism of patients. Here we examined the effects of sexual dimorphism on therapeutic agent efficiencies in murine models. High-throughput sequencing of host mRNA showed that different treatments reprogrammed the spectrum of mRNA expression in small intestines of male or female mice, respectively. Collectively, our observations demonstrate that therapeutic strategy efficiencies for radiation toxicity might be dependent on the gender of patients. We aim to uncover the underlying mechanisms by which simvastatin or high fat diet fights against radiotherapy-induced gastrointestinal tract toxicity for male or female mice. The mice were exposed to 12 Gy total abdominal irradiation (TAI), then treated with simvastatin for male mice or fed with high fat diet for female mice. The small intestine tissues were extracted from male mice without TAI, exposed to TAI only, and exposed to TAI combined with simvastatin treatment as one cohort, and from female mice without TAI, exposed to TAI only, and exposed to TAI combined with high fat diet feeding as the other cohort.
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Project description:Accidental or iatrogenic ionizing radiation exposure precipitates acute and chronic radiation injuries. Traditional paradigm of mitigating radiotherapy-associated side effects has ignored the gender-specific dimorphism of patients. Here we examined the effects of sexual dimorphism on therapeutic agent efficiencies in murine models. High-throughput sequencing showed that different treatments preserved miRNA expression profile in small intestines of male or female mice, respectively. Collectively, our observations demonstrate that therapeutic strategy efficiencies for radiation toxicity might be dependent on the gender of patients. We aim to uncover the underlying mechanisms by which simvastatin or high fat diet fights against radiotherapy-induced gastrointestinal tract toxicity for male or female mice. The mice were exposed to 12 Gy total abdominal irradiation (TAI), then treated with simvastatin for male mice or fed with high fat diet for female mice. The small intestine tissues were extracted from male mice without TAI, exposed to TAI only, and exposed to TAI combined with simvastatin treatment as one cohort, and from female mice without TAI, exposed to TAI only, and exposed to TAI combined with high fat diet feeding as the other cohort.
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