Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1105342 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:RNAseq of intestinal epithelial cells from ASF Mice colonized with a consortium of mucosa associated fungi
2021-12-30 | GSE141622 | GEO
Project description:Interventions: healthy people, intestinal polyp group and intestinal cancer group.:Nil
Primary outcome(s): bacteria;fungi;phages
Study Design: Factorial
| 2702334 | ecrin-mdr-crc
Project description:To examine potential changes of the intestinal microbiota in mice caused by repeated mild stress, we profiled bacteria and fungi in the mouse feces by sequencing the 16s v3v4 region and the ITS1-2 region.
2024-09-23 | GSE222533 | GEO
Project description:Interventions: Case series:None
Primary outcome(s): intestinal fungi
Study Design: Sequential
| 35158 | ecrin-mdr-crc
Project description:Interventions: Gold Standard:pathological examination;Index test:new colorectal cancer screening kit
Primary outcome(s): Intestinal bacteria;Intestinal fungi;Intestinal virus
Study Design: Sequential
| 2726246 | ecrin-mdr-crc
Project description:Recent studies demonstrate that the gut mycobiota plays a key role in several tumors’ development. However, the contribution of commensal fungi to prostate cancer initiation and progression remains understudied. Here, we find that Nakaseomyces glabratus (N.glabratus), is enriched in fecal, blood, and tumor samples of a subset of CRPC patients, positively correlating with patients’ poor overall survival. Oral administration of N.glabratus to castrated mice accelerated CRPC development by controlling polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). Mechanistically, androgen deprivation therapy (ADT) increases intestinal permeability, resulting in the leakage of N.glabratus from the gut to the tumor site, where it activates PMN-MDSCs by binding to the Dectin-2 receptor. Treatment of mice with a negatively charged hydrogel blocks N.glabratus translocation to the tumor site, reducing PMN-MDSCs intratumoral infiltration and activation. Taken together, these findings reveal that the gut-to-tumor translocation of commensal fungi contributes to endocrine resistance in CRPC by enhancing the immunosuppressive microenvironment of these tumors.
2025-12-02 | GSE311900 | GEO
Project description:The development and severity of inflammatory bowel diseases (IBD) and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that intestinal epithelial cells (IECs) isolated from IBD patients exhibit decreased expression of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3). Further, genome-wide analyses of murine IECs that lack HDAC3 (HDAC3ΔIEC) revealed that HDAC3 deficiency resulted in dysregulated gene expression coupled with alterations in histone acetylation. Critically, conventionally-housed HDAC3ΔIEC mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3ΔIEC mice exhibited significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 plays a central role in maintaining intestinal homeostasis. Strikingly, rederivation of HDAC3ΔIEC mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis, and intestinal barrier function were largely restored in the absence of commensal bacteria. Collectively, these data indicate that the HDAC3 is a critical factor that integrates commensal bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis. Analyses of histone acetylation in primary IECs from HDAC3FF (3 biologic replicates) and HDAC3ΔIEC (3 biologic replicates) mice were conducted utilizing ChIP-seq for H3K9Ac.
2013-12-02 | E-GEOD-50453 | biostudies-arrayexpress