Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1283483 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Intestinal microbiota diversity of two commercially valuable freshwater fish species
| PRJDB3256 | ENA
Project description:Endemic Schizothoracinae fish strain:adult | breed:wild Assembly
| PRJNA576106 | ENA
Project description:Intestinal Foxp3+ regulatory T cell (Treg) subsets are crucial players for tolerance towards microbiota-derived and food-borne antigens, and compelling evidence suggests that intestinal microbiota modulate their differentiation and maintenance. Selected bacterial species and microbiota-derived metabolites such as short-chain fatty acids (SCFAs) have been reported to foster Treg homeostasis in the intestinal lamina propria. Furthermore, gut-draining mesenteric lymph nodes (mLNs) are particularly efficient sites of de novo Treg induction, and we could previously show that mLN stromal cells contribute to this process. Yet, it is not fully elucidated which direct role microbiota and their metabolites play for the early stages of de novo Treg induction and in shaping the Treg transcriptome already during the initial priming within mLNs. Here, we show that neither dysbiotic microbiota nor dietary SCFA supplementation impact de novo induction of Foxp3+ Tregs within mLNs. Even mice housed under germ-free (GF) conditions displayed equivalent frequencies of de novo induced Foxp3+ Tregs within mLNs. Further dissection of the accessible chromatin and transcriptome revealed that microbiota indeed have a limited impact on fostering the establishment of peripherally induced Tregs and do not contribute to the initialization of the epigenetic landscape for an extensive Treg signature. Viewed as a whole, our data suggest that microbiota are dispensable for the early stages of de novo Treg induction within mLNs, while being required to foster further Treg differentiation and homeostasis at later stages within the intestinal lamina propria.
2021-03-24 | GSE150566 | GEO
Project description:intestinal microbiota of fish Metagenome
| PRJNA493193 | 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:Intestinal innate lymphoid cells (ILCs) contribute to the protective immunity and homeostasis of the gut, and the microbiota are critically involved in shaping ILC function. However, the role of the gut microbiota in regulating ILC development and maintenance still remains elusive. Here, we identified opposing effects on ILCs by two Helicobacter species, Helicobacter apodemus and Helicobacter typhlonius, isolated from immunocompromised mice. We demonstrated that the introduction of both Helicobacter species activated ILCs and induced gut inflammation; however, these Helicobacter species negatively regulated RORγt+ Group 3 ILCs (ILC3s), especially T-bet+ ILC3s, and diminished their proliferative capacity. Thus, these findings underscore a previously unknown dichotomous regulation of ILC3s by Helicobacter species, and may serve as a model for further investigations to elucidate the host-microbe interactions that critically sustain the maintenance of intestinal ILC3s.
2019-11-18 | GSE136171 | GEO