Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1051022 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27172976_1.fastq.gz | Fastqsanger.gz | |||
| SRR27172976_2.fastq.gz | Fastqsanger.gz | |||
| SRR27172977_1.fastq.gz | Fastqsanger.gz | |||
| SRR27172977_2.fastq.gz | Fastqsanger.gz | |||
| SRR27172978_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:It has been shown in vitro that only specific dietary-fibers contribute to immunity but studies in vivo are not conclusive. Here we investigated degree of polymerization (DP) dependent effects of β2→1-fructans on immunity via microbiota-dependent and -independent effects. To this end, conventional or germ-free mice received short- or long-chain β2→1-fructan for 5 days. Immune cell populations in the spleen, mesenteric lymph nodes (MLN), and Peyer's patches (PPs) were analyzed with flow cytometry, genome-wide gene expression in the ileum was measured with microarray, and gut microbiota composition was analyzed with 16S rRNA sequencing of fecal samples. We found that β2→1-fructans modulated immunity by both microbiota and microbiota-independent effects. Moreover, effects were dependent on the chain-length of the β2→1-fructans type polymer. Both short- and long-chain β2→1-fructans enhanced T-helper 1 cells in Peyer's patches, whereas only short-chain β2→1-fructans increased regulatory T cells and CD11b-CD103- DCs in the MLN. A common feature after short- and long-chain β2→1-fructan treatment was enhanced Fut2 expression and other IL-22-dependent genes in the ileum of conventional mice. These effects were not associated with shifts in gut microbiota composition, or altered production of short-chain fatty acids. Both short- and long-chain β2→1-fructans also induced immune effects in germ-free animals, demonstrating direct effect independent from the gut microbiota. Also, these effects were dependent on the chain-length of the β2→1-fructans. Short-chain β2→1-fructan induced lower CD80 expression by CD11b-CD103- DCs in PPs, whereas long-chain β2→1-fructan specifically modulated B cell responses in germ-free mice. In conclusion, support of immunity is determined by the chemical structure of β2→1-fructans and is partially microbiota-independent.
2018-03-22 | GSE94516 | GEO
Project description:Studying host-microbiota interactions is fundamental to understand mechanisms involved in intestinal inflammation and inflammatory bowel diseases. In this work, we studied these interactions in mice mono-associated with 4 bacteria and 2 yeasts, all representative of intestinal microbiota and/or associated with IBD pathogenesis: Bacteroides thetaiotaomicron, adhesive-invasive Escherichia coli (AIEC), Ruminococcus gnavus, Roseburia intestinalis, Saccharomyces boulardii and Candida albicans. Transcriptomics analyses showed that B. thetaiotaomicron had the highest immunological effect, being able to almost recapitulate the effects of a whole microbiota, and particularly induced Treg pathways. Furthermore, this analysis also pointed out the effects of E. coli AIEC LF82 on IDO activation and of S. boulardii on angiogenesis, as well as major effects of R. gnavus on metabolism. This work therefore reveals information on the role of each micro-organism and proposes several tracks to follow to better understand IBD pathogenesis and identify therapeutic targets 6 mono-associations + 2 controls (germ-free and conventionalized mice), with 5 to 7 mice per group.
2015-08-22 | E-GEOD-63299 | biostudies-arrayexpress
Project description:The interplay between the intestinal microbiota and host is critical to intestinal ontogeny and homeostasis. MicroRNAs (miRNAs) may be an underlying link. Intestinal miRNAs are microbiota-dependent and when shed in the lumen, affect resident microorganisms. Yet, longitudinal relationships between intestinal tissue miRNAs, luminal miRNAs, and luminal microorganisms have not been elucidated, especially in early life. Here, we investigated the postnatal cecal miRNA and microbiota populations, their relationship, and their impact on intestinal maturation in specific and opportunistic pathogen free mice; we also assessed if they can be modified by an intervention with allochthonous probiotic lactobacilli. We report that cecal and cecal content miRNA and microbiota signatures are temporally regulated, correlated, and modifiable by probiotics with implications for intestinal maturation. These findings help with understanding causal relationships within the gut ecosystem and provide a basis for preventing and managing their alterations in diseases throughout life.
2023-07-08 | GSE149418 | GEO
Project description:A striking example of the intricate interplay between diet, microbiota, and host is the effect of inulin, a dietary fiber, on the intestinal epithelium. Ingestion of inulin triggers a wide range of epithelial effects in the colon, such as enhanced proliferation, increased production of mucus and antimicrobial peptides, as well as systemic effects on host metabolism and immune function that are dependent on microbiota-derived molecules. In this study, we investigated the impact of inulin on two critical aspects of diet-microbiota-host interactions: intestinal hypoxia and the modulation of hypoxia-inducible factor (HIF)-1 signaling in intestinal epithelial cells (IECs) in mice colon. To achieve this, we employed a multilayered and multi-omics approach, including dietary interventions, in vitro analysis using intestinal organoids, and both genetic and pharmacological interventions. We found that inulin intake enhances intestinal hypoxia, resulting in the stabilization of HIF-1 in IECs, an effect that is both microbiota- and host-dependent. Our study revealed that HIF-1 plays a key role in regulating IEC proliferation and intestinal stem cell (ISC) function. These changes are associated with HIF-1-dependent metabolic alterations in IECs. Our findings uncover a novel mechanism by which HIF-1 acts in the colon: it acts as a molecular brake, modulating cell proliferation in a microbiota-dependent manner and through metabolic reprogramming, highlighting the complexity of the diet-microbiota-host interactions in the gut.
2025-08-22 | PXD059757 | Pride
Project description:A dysbiosis in the intestinal microbiome plays a role in the pathogenesis of several immunological diseases. These diseases often show a gender bias, suggesting gender differences in immune responses and in the intestinal microbiome. We hypothesized that gender differences in immune responses are associated with gender differences in microbiota. We demonstrated mouse strain dependent gender differences in the intestinal microbiome. Interestingly, a cluster of colonic genes (related to humoral and cell-mediated immune responses) correlated oppositely with microbiota species abundant in B6 females and in BALB/c males. This suggests that with different genetic backgrounds, gender associated immune responses are differentially regulated by microbiota. The net result was the same, since both mouse strains showed similar gender induced differences in immune cell populations in the mesenteric lymph nodes. Therefore, host-microbe interactions might be more complicated than assumed, as bacterial-species adaptations might be highly dependent on the genetic make-up of the individual.
2018-06-27 | GSE85911 | GEO
Project description:A dysbiosis in the intestinal microbiome plays a role in the pathogenesis of several immunological diseases. These diseases often show a gender bias, suggesting gender differences in immune responses and in the intestinal microbiome. We hypothesized that gender differences in immune responses are associated with gender differences in microbiota. We demonstrated mouse strain dependent gender differences in the intestinal microbiome. Interestingly, a cluster of colonic genes (related to humoral and cell-mediated immune responses) correlated oppositely with microbiota species abundant in B6 females and in BALB/c males. This suggests that with different genetic backgrounds, gender associated immune responses are differentially regulated by microbiota. The net result was the same, since both mouse strains showed similar gender induced differences in immune cell populations in the mesenteric lymph nodes. Therefore, host-microbe interactions might be more complicated than assumed, as bacterial-species adaptations might be highly dependent on the genetic make-up of the individual.
2018-06-27 | GSE85912 | GEO
Project description:The importance of the mammalian intestinal microbiota to human health has been intensely studied over the past few years. It is now clear that the interactions between human hosts and their associated microbial communities need to be characterized in molecular detail if we are to truly understand human physiology. Additionally, the study of such host-microbe interactions is likely to provide us with new strategies to manipulate such complex systems to maintain or restore homeostasis in order to prevent or cure pathological states. We describe the use of high-throughput metabolomics to shed light on the interactions between the intestinal microbiota and the host. We show that treatment with the antibiotic streptomycin disrupts intestinal homeostasis and has a profound impact on the intestinal metabolome, affecting the levels of over 87% of all metabolites detected. Many metabolic pathways that are critical for host physiology were affected, including bile acid, eicosanoid and steroid hormone synthesis. Interestingly, many of these pathways are also affected by intestinal pathogens. Dissecting the effect of both beneficial and pathogenic bacteria on some of these pathways will be instrumental in understanding the interplay between the host, the resident microbiota and incoming pathogens and may aid in the design of new therapeutic strategies that target these interactions.
2011-02-08 | GSE25687 | GEO
Project description:The impact of microbial colonization during early life on immune system development and host health is well-established. Therefore, we investigated whether alterations in the intestinal microbiota resulting from cesarean section (CS) would affect the colonic immune system.
2023-11-22 | GSE231473 | GEO
Project description:Major depressive disorder is caused by gene-environment interactions and the gut microbiota plays a pivotal role in the development of depression. However, the mechanisms by which the gut microbiota modulates depression remain elusive. Herein, we detected the differentially expressed hippocampal long non-coding RNAs (lncRNAs), messenger RNAs (mRNAs) and microRNAs (miRNAs) between mice inoculated with gut microbiota from major depressive disorder patients or healthy controls, to identify the effects of gut microbiota-dysbiosis on gene regulation patterns at the transcriptome level. We also performed functional analysis to explore the microbial-regulated pathological mechanisms of depression. Two hundred mRNAs, 358 lncRNAs and 4 miRNAs were differentially expressed between the two groups. Functional analysis of these differentially expressed mRNAs indicated dysregulated inflammatory response to be the primary pathological change. Intersecting the differentially expressed mRNAs with targets of differentially expressed miRNAs identified 47 intersected mRNAs, which were mainly related to neurodevelopment. Additionally, we constructed a microbial-regulated lncRNA-miRNA-mRNA network based on RNA-RNA interactions. According to the competitive endogenous RNA hypothesis, two neurodevelopmental ceRNA sub-networks implicating in depression were identified. This study provides new understanding of the pathogenesis of depression induced by gut microbiota-dysbiosis and may act as a theoretical basis for the development of gut microbiota-based antidepressants.
2021-12-31 | GSE189159 | GEO