Mouse gut microbiota
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA634807 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11856700_1.fastq.gz | Fastqsanger.gz | |||
| SRR11856700_2.fastq.gz | Fastqsanger.gz | |||
| SRR11856701_1.fastq.gz | Fastqsanger.gz | |||
| SRR11856701_2.fastq.gz | Fastqsanger.gz | |||
| SRR11856702_1.fastq.gz | Fastqsanger.gz |
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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.
2020-02-17 | PXD016099 | Pride
Project description:In the presented study, in order to unravel gut microbial community multiplicity and the influence of maternal milk nutrients (i.e., IgA) on gut mucosal microbiota onset and shaping, a mouse GM (MGM) was used as newborn study model to discuss genetic background and feeding modulation on gut microbiota in term of symbiosis, dysbiosis and rebiosis maintenance during early gut microbiota onset and programming after birth. Particularly, a bottom-up shotgun metaproteomic approach, combined with a computational pipeline, has been compred with a culturomics analysis of mouse gut microbiota, obtained by MALDI-TOF mass spectrometry (MS).
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Project description:Acarbose was reported to alleviate obesity-induced insulin resistance IR and regulate the gut microbiota community; however, the critical microbial signaling metabolites and the host targets associated with the metabolic benefits of acarbose remains unknown. In this study, we reported that acarbose treatment was able to significantly improve high fat diet (HFD) induced IR and inflammation states in adipose tissue and intestine by influencing the survival and pro-inflammatory function of M1 macrophages. Furthermore, we revealed that acarbose exert anti-inflammatory effects partly in a gut-microbiota dependent manner by microbiota clearance experiments. 16S rRNA sequencing and metabolomic researches identified that acarbose could enhance the proliferation of propionic acid (PA)-producing Parasutterella excrementihominis (PARA). As the vital metabolic mediator, PA regulated the pro-inflammatory and anti-inflammatory balance of M1/M2 macrophages by GPR4/NLRP3 signaling pathway. In addition, in vivo studies of NBD fluorescence labeled acarbose verified that acarbose directly inhibited the macrophage inflammatory response in adipose tissue via being captured by intestinal macrophage due to the aggravated intestinal permeability in HFD mice. We also validated this result in bone-marrow derived macrophage (BMDM) and human macrophages in vitro. Mechanistically, acarbose may suppressed mTOR signaling pathway and the following autophagy/mitochondrial function of M1 macrophage by activating GPR120, thereby reducing its survival and the secretion of pro-inflammatory cytokines. In conclusion, these findings presented that acarbose improved obesity-induced IR by maintaining beneficial microbiota and direct inhibited action on M1 macrophages.
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Project description:Lactobacillus rhamnosus ameliorated the pro-inflammatory process in DIO mice.
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Project description:In this study we performed MeRIP-Seq to study N6-methyl adenosine (m6A) and and N6,2′ -O-dimethyladenosine (m6Am) modification of mRNA. We investigated the effect of the microbiota on the transcriptome and epitranscriptomic modifications in murine liver and cecum. We compared m6A/m modification profiles in cecum of conventionally raised (CONV) and germ-free (GF) mice. We additionally included GF mice colonised with the flora of CONV mice for four weeks (ex-GF), for which show that they exhibit similar patterns of the most abundant genera of gut bacteria as CONV mice. We added mice treated with several antibiotics to deplete the gut flora (abx)and vancomycin treated mice in which the genera Akkermansia, Escherichia/Shigella and Lactobacillus were enriched. Furthermore, we included GF mice colonised with the commensal bacterium Akkermansia muciniphila (Am), Lactobacillus plantarum (Lp) and Escherichia coli Nissle (Ec) and analysed their m6A/m modification profiles. In addition, we analysed changes in m6A/m- modified liver RNA for CONV, GF, and Am, Lp and Ec mice.
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Project description:Early-weaning-induced stress causes diarrhea, thereby reduces growth performance of piglets. Gut bacterial dysbiosis emerges as a leading cause of post-weaning diarrhea. The present study was aimed to investigate the effect of capsulized fecal microbiota transportation (FMT) on gut bacterial community, immune response and gut barrier function of weaned piglets. Thirty-two were randomly divided into two groups fed with basal diet for 21 days. Recipient group was inoculated orally with capsulized fecal microbiota of health Tibetan pig daily morning during whole period of trial, while control group was given orally empty capsule. The results showed that the F/G ratio, diarrhea ratio, diarrhea index, and histological damage score of recipient piglets were significantly decreased. FMT treatment also significantly increased the colon length of piglets. Furthermore, the relative abundances of Firmicutes, Euryarchaeota, Tenericutes, Lactobacillus, Methanobrevibacter and Sarcina in colon of recipient piglets were increased, and the relative abundances of Campylobacter, Proteobacteria, and Melainabacteria were significantly decreased compared with control group.
2019-09-17 | GSE137470 | GEO
Project description:Microbial sequencing revealed progressive reduction of gut microbiota that showed some differences in the two ABX groups compared to untreated controls. Interestingly, duration of ABX was associated with a gradual disappearance of the CD4+ and CD4+CD8+ subset of gut intraepithelial lymphocytes (IELs). This IEL subset is microbiota-dependent and is absent in germ-free mice. Relative abundance of Lactobacillus reuteri correlated with frequencies of CD4+CD8+ IELs and reduced EAU. Notably, IELs in culture suppressed antigen-specific activation of autoreactive T cells.
2023-11-17 | GSE236922 | GEO
Project description:Depressive disorders often run in families, which, in addition to the genetic component, may point to the microbiome as a causative agent. Here, we employed a combination of behavioral, molecular and computational techniques to test the role of the microbiota in mediating despair behavior. In chronically stressed mice displaying despair behavior, we found that the microbiota composition and the metabolic signature dramatically change. Specifically, we observed reduced Lactobacillus and increased circulating kynurenine levels as the most prominent changes in stressed mice. Restoring intestinal Lactobacillus levels was sufficient to improve the metabolic alterations and behavioral abnormalities. Mechanistically, we identified that Lactobacillus-derived reactive oxygen species may suppress host kynurenine metabolism, by inhibiting the expression of the metabolizing enzyme, IDO1, in the intestine. Moreover, maintaining elevated kynurenine levels during Lactobacillus supplementation diminished the treatment benefits. Collectively, our data provide a mechanistic scenario for how a microbiota player (Lactobacillus) may contribute to regulating metabolism and resilience during stress.
2020-07-08 | GSE153992 | GEO
Project description:At birth, newborns are exposed to gut microbiota, which plays a critical role in host physiology. A reduced level of microbial diversity has been associated with necrotizing enterocolitis (NEC), one of the most deadly diseases in premature infants, but the underlying disease mechanisms are still poorly understood. Although the epithelial turnover of germ free mice is significantly delayed compared to conventionally raised mice, it remains unclear how gut microbiota exposure in the early postnatal period promotes stem cell renewal and differentiation. By analyzing genetic and experimental mouse models and performing single cell analysis, we demonstrate that gut microbiota promotes stem cell differentiation through the activation of critical stromal niche components. Our single cell analysis reveals that gut microbiota controls the size and heterogeneity of macrophage populations that secrete Wnt ligands, thereby maintaining the proliferation of intestinal telocytes, a recently identified gut mesenchymal stem cell niche. We show that stem cell differentiation, when impaired by antibiotic treatment promotes NEC, while treatment with Lactobacillus, which in NEC is dramatically less abundant, rescues NEC-like pathology through the activation of macrophage and telocyte niches. Our work highlights the mechanisms of how gut microbiota-facilitate mesenchymal niche proliferation which supports stem cell differentiation in early postnatal development.
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Project description:Purpose: Gut microbiota is associated with the progression of brain tumor. However, the alterations in the gut microbiota during glioma growth and temozolomide (TMZ) therapy remains to be understood. Methods: C57BL/6 male mice were implanted with GL261 glioma cells. TMZ/sodium carboxymethyl cellulose (SCC) was administered by gavage for five consecutive days (from 8 to 12 days after implantation). Fecal samples were collected before (T0) and on days 7 (T1), 14 (T2), and 28 (T3) after implantation. The gut microbiota was analyzed using 16S ribosomal DNA sequencing followed by absolute and relative quantitation analyses. Results: Nineteen genera were altered during glioma progression with the most dramatic changes in Firmicutes and Bacteroidetes phyla. During glioma growth, Lactobacillus abundance decreased at the earlier stage of glioma development (T1), and then gradually increased (T2, T3); Intestinimonas abundance exhibited a persistent increase; Anaerotruncus showed a transient increase and then a subsequent decrease. Twenty genera altered following TMZ treatment. The enrichment of Akkermansia and Bifidobacterium was observed only at the early stage following TMZ treatment (T2), but not at the later stage (T3). Additionally, the decrease of Anaerotruncus was slighter in TMZ group at T3 comparing to the vehicle group. The abundance of Intestinimonas increased constantly during the progression of glioma, but was unaffected by TMZ. Conclusions: Glioma development and progression resulted in altered gut microbiota. TMZ reversed the decrease of Anaerotruncus in glioma at T3, and increased the abundance of Bifidobacterium with no influence on the increase of Intestinimonas. Short-term and long-term effects of TMZ treatment on the bacterial communities may be differential. This study will improve understanding the role of gut microbiota in glioma, and help develop gut microbiota as a potential therapeutic target.
2021-04-28 | GSE171041 | GEO