Ontology highlight
ABSTRACT:
PROVIDER: PRJNA342805 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4240990.fastq.gz | Fastqsanger.gz | |||
| SRR4241000.fastq.gz | Fastqsanger.gz | |||
| SRR4241010.fastq.gz | Fastqsanger.gz | |||
| SRR4241030.fastq.gz | Fastqsanger.gz | |||
| SRR4241050.fastq.gz | Fastqsanger.gz |
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Project description:Microbiota-induced cytokine responses participate in gut homeostasis, but the cytokine balance at steady-state and the role of individual bacterial species in setting the balance remain elusive. Using gnotobiotic mouse models, we provide a systematic analysis of the role of microbiota in the induction of cytokine responses in the normal intestine. Colonization by a whole mouse microbiota orchestrated a broad spectrum of pro-inflammatory (Th1, Th17) and regulatory T cell responses. Unexpectedly, most tested complex microbiota and individual bacteria failed to efficiently stimulate intestinal cytokine responses. A potent cytokine-inducing function was however associated with non-culturable host-specific species, the prototype of which was the Clostridia-related Segmented Filamentous Bacterium, and this bacterial species recapitulated the coordinated maturation of T cell responses induced by the whole mouse microbiota. Our study demonstrates the non-redundant role of microbiota members in the regulation of gut immune homeostasis. Germfree (GF) female 8-9-week-old mice were gavaged twice at a 24-hr interval with 0.5 mL of fresh anaerobic cultures of fecal homogenate from SFB mono-associated mice, fresh feces from Cv mice (Cvd) or from a healthy human donor (Hum). All mice were sacrificed on d8, 20 and 60 post-colonization in parallel to age-matched Cv and GF controls. RNA was extracted from ileal tissue, and processed to biotin-labelled cRNA, and then hybridized to the NuGO array (mouse) NuGO_Mm1a520177. Microarray analysis compared gene expression in ileum tissue of all the treatment groups GF, Cv, Cvd, Hum and SFB (N=3 per treatment group per time-point). Data was considered significant when P<0.05 using the Benjamini and Hochberg false discovery method.
2010-05-05 | E-GEOD-18056 | biostudies-arrayexpress
Project description:Microbiota-induced cytokine responses participate in gut homeostasis, but the cytokine balance at steady-state and the role of individual bacterial species in setting the balance remain elusive. Using gnotobiotic mouse models, we provide a systematic analysis of the role of microbiota in the induction of cytokine responses in the normal intestine. Colonization by a whole mouse microbiota orchestrated a broad spectrum of pro-inflammatory (Th1, Th17) and regulatory T cell responses. Unexpectedly, most tested complex microbiota and individual bacteria failed to efficiently stimulate intestinal cytokine responses. A potent cytokine-inducing function was however associated with non-culturable host-specific species, the prototype of which was the Clostridia-related Segmented Filamentous Bacterium, and this bacterial species recapitulated the coordinated maturation of T cell responses induced by the whole mouse microbiota. Our study demonstrates the non-redundant role of microbiota members in the regulation of gut immune homeostasis.
2009-09-11 | GSE18056 | GEO
Project description:Parkinson's disease (PD) is a common neurodegenerative disease in middle-aged and elderly people. The disorder of gut microbiota is involved in the pathophysiological process of various neurological diseases, and many studies have confirmed that gut microbiota is involved in the progression of PD. As one of the most effective methods to reconstruct gut microbiota, fecal microbiota transplantation (FMT) has been considered as an important treatment for PD. However, the mechanism of FMT treatment for PD is still lacking, which requires further exploration and can facilitate the application of FMT. As a model organism, Drosophila is highly conserved with mammalian system in maintaining intestinal homeostasis. In this study, there were significant differences in the gut microbiota of conventional Drosophila colonized from PD patients compared to those transplanted from normal controls. And we constructed rotenone-induced PD model in Drosophila followed by FMT in different groups, and investigated the impact of gut microbiome on transcriptome of the PD host. Microbial analysis by 16S rDNA sequencing showed that gut microbiota could affect bacterial structure of PD, which was confirmed by bacterial colonization results. In addition, transcriptome data suggested that gut microbiota can influence gene expression pattern of PD. Further experimental validations confirmed that lysosome and neuroactive ligand-receptor interaction are the most significantly influenced functional pathways by PD-derived gut microbiota. In summary, our data reveals the influence of PD-derived gut microbiota on host transcriptome and helps better understanding the interaction between gut microbiota and PD through gut-brain axis. The present study will facilitate the understanding of the mechanism underlying PD treatment with FMT in clinical practice.
2023-01-13 | GSE221760 | GEO
Project description:We transplanted gut microbiota via fecal transfer from TD and ASD children into germ-free wild-type mice, and reveal that colonization with ASD microbiomes induces hallmark changes in sociability, vocalization, and stereotypies. The brains of mice receiving gut microbiota from ASD individuals display alternative splicing patterns for genes dysregulated in the human ASD brain.
2019-02-01 | GSE109827 | GEO
Project description:Here, we report analysis of both the bacterial and host transcriptome as affected by colonization of R. hominis in the mouse gut. Microbial genes required for colonization and adaptation in the murine gut, as well as host genes responding to colonization by this bacterial species, were uncovered.
2016-02-05 | GSE25544 | GEO
Project description:The mammalian gut harbors a diverse microbial community (gut microbiota) that mainly consists of bacteria. Their combined genomes (the microbiome) provide biochemical and metabolic functions that complement host physiology. Maintaining symbiosis seems to be a key requirement for health as dysbiosis is associated with the development of common diseases. Previous studies indicated that the microbiota and the hostM-bM-^@M-^Ys epithelium signal bidirectional inducing transcriptional responses to fine-tune and maintain symbiosis. However, little is known about the hostM-bM-^@M-^Ys responses to the microbiota along the length of the gut as earlier studies of gut microbial ecology mostly used either colonic or fecal samples. This is of importance as not only function and architecture of the gut varies along its length but also microbial distribution and diversity. Few recent studies have begun to investigate microbiota-induced host responses along the length of the gut. However, these reports used whole tissue samples and therefore do not allow drawing conclusions about specificity of the observed responses. Which cells in the intestinal tissue are responsible for the microbially induced response: epithelial, mesenchymal or immune cells? Where are the responding cells located? Furthermore, the gut microbiota has been implicated in epigenetic regulation of the hostM-bM-^@M-^Ys transcriptional profile. We used using extensive microarray analysis of laser capture microdissection (LCM) harvested ileal and colonic tip and crypt fractions from germ-free mice before and during the time course of colonization with a normal microbiota (on days 1, 3, 5 and 7) to investigate the microbiota-induced transcriptional responses and their kinetics in specific and well-defined cell populations of the hostM-bM-^@M-^Ys epithelium. Ileum and colon segments were dissected from germ-free 10-12 weeks old female C57Bl/6 mice and on day 1, 3, 5 and 7 after colonization, washed and frozen as OCT blocks. Cryosections were prepared from these OCT blocks and tip/crypt fractions isolated using laser capture microdissection. To investigate the microbiota-induced transcriptional responses specific for specific subpopulations of intestinal epithelial cells and their kinetics, tip and crypt fractions of ileal and colonic epithelium of germ-free 10-12 weeks old female C57Bl/6 mice before and during the time course of colonization with a normal microbiota (on days 1, 3, 5 and 7) were harvested using laser capture microdissection and probed in an extensive microarray analysis.
2015-02-12 | E-GEOD-51911 | biostudies-arrayexpress
Project description:Colonizing commensal bacteria after birth are required for the proper development of the gastrointestinal tract. It is believed that bacterial colonization pattern in neonatal gut affects gut barrier function and immune system maturation. Studies on the development of faecal flora microbiota in infants on various formula feeds showed that the neonatal gut was first colonized with enterococci followed by other flora microbiota such as Bifidobacterium in breast feeding infants. Intriguingly, Bjorksten group Other studies showed that Bbabies who developed allergy were less often colonized with Enterococcus during the first month of life as compared to healthy infants. A lot of Many studies have been done on conducted to elucidate how bifidobacteria or lactobacilli, some of which are considered probiotic, regulate infant gut immunity. However, much fewer studies have been focused on enterococi. In our study, we demonstrate that E. faecalis, isolated from healthy newborns, suppress inflammatory responses activated in vivo and in vitro. We found E. faecalis attenuates proinflammatory cytokine secretions, especially IL-8, through JNK and p38 signaling pathways. This finding shed light on how the first colonizer, E.faecalis, regulate inflammatory responses in the host. Samples are analysed using web-based GEArray Expression Analysis Suite
2014-04-04 | E-GEOD-56485 | biostudies-arrayexpress
Project description:Gut-microbiota membership is associated with diverse neuropsychological-diseases, including substance use disorders (SUDs). Unravelling mechanistic interactions between gut microbes and the host during psychostimulant use remains challenging. Here we show that cocaine exposure increases intestinal levels of norepinephrine, sensed through the bacterial adrenergic receptor QseC, promoting intestinal colonization of g-Proteobacteria. Gut colonization by g-Proteobacteria depletes the neuroactive metabolite glycine (used as a nitrogen source) both in the gut and cerebrospinal fluid, enhancing host cocaine-induced behaviors. Glycine repletion reversed this response, and intestinal colonization by g-Proteobacteria unable to uptake glycine did not alter the host response to cocaine. Transcriptomic profiling indicates a role of g-Proteobacteria modulated glycine levels in cocaine induced transcriptional plasticity in the nucleus accumbens through the glutamatergic transmission. Altogether, we introduce a mechanism by which intestinal bacteria alter the host’s brain responses to cocaine that could be exploited to modulate reward-related brain circuits that contribute to SUDs.
2022-09-07 | GSE212421 | GEO
Project description:To characterize the effect of microbiota on global gene expression in the distal small intestine during postnatal gut development we employed mouse models with experimental colonization by intestinal microbiota. Using microarray analysis to assess global gene expression in ileal mucosa at the critical stage of intestinal development /maturation associated with weaning, and asking how expression is affected by microbial colonization In the study presented here, preweaned and postweaned GF, SPF mouse small intestinal total RNAs were used. Also, 3-week-old gnotobiotic mouse as well as GF mouse small intestinal RNAs were used.
2013-03-02 | E-GEOD-44788 | biostudies-arrayexpress
Project description:The adult human gut microbial community is typically dominated by two bacterial phyla (divisions), the Firmicutes and the Bacteroidetes. Little is known about the factors that govern the interactions between their members. Here we examine the niches of representatives of both phyla in vivo. Finished genome sequences were generated from E. rectale and E. eligens, which belong to Clostridium Cluster XIVa, one of the most common gut Firmicute clades. Comparison of these and 25 other gut Firmicutes and Bacteroidetes indicated that the former possess smaller genomes and a disproportionately smaller number of glycan-degrading enzymes. Germ-free mice were then colonized with E. rectale and/or a prominent human gut Bacteroidetes, Bacteroides thetaiotaomicron, followed by whole genome transcriptional profiling of both organisms in their distal gut (cecal) habitat as well as host responses, high resolution proteomic analysis of cecal contents, and biochemical assays of carbohydrate metabolism. B. thetaiotaomicron adapts to E. rectale by upregulating expression of a variety of polysaccharide utilization loci (PULs) encoding numerous glycoside hydrolase gene families, and by signaling the host to produce mucosal glycans that it, but not E. rectale, can access. E. rectale adapts to B. thetaiotaomicron by decreasing production of its glycan-degrading enzymes, increasing expression of selected amino acid and sugar transporters, and facilitating glycolysis by reducing levels of NADH, in part via generation of butyrate from acetate, which in turn is utilized by the gut epithelium. This simplified model of the human gut microbiota illustrates niche specialization and functional redundancy within members of major gut bacterial phyla, and the importance of host glycans as a nutrient foundation that ensures ecosystem stability. The interactions between E. rectale and B. thetaiotaomicron were characterized by performing whole genome transcriptional profiling of each species after colonization of gnotobiotic mice with each organism alone, or in combination. E. rectale was also profiled during in vitro growth.
2010-05-22 | E-GEOD-14737 | biostudies-arrayexpress