Wildmice Microbiome and mycobiome analysis
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB65584 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR11939300_1.fastq.gz | Fastqsanger.gz | |||
| ERR11939300_2.fastq.gz | Fastqsanger.gz | |||
| ERR11939301_1.fastq.gz | Fastqsanger.gz | |||
| ERR11939301_2.fastq.gz | Fastqsanger.gz | |||
| ERR11939302_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 98 |
Similar Datasets
Project description:Acute graft-vs-host disease (aGVHD) can affect the central nervous system (CNS) through activation of microglia and infiltration of T cells. However, it is unclear how microbiome modifications impact CNS-aGVHD. Here, we analyzed the role of the microbiome in facilitating microglia activation during aGVHD using antibiotics-treated, germ-free (GF) and wildling mice. Antibiotics-mediated microbiome depletion caused infiltration of IFN-γ producing T cells in the brain, activation of microglia via the TLR4/p38MAPK pathway and deficits in neurocognitive functions in aGVHD mice. We observed similar microbiome-dependent microglia activation after allo-HCT in microbiome-disrupted wildling mice, and in GF mice compared to Oligo-Mouse-Microbiota (OMM12) mice. The bacteria-derived metabolite N,N,N-trimethyl-5-aminovalerate (TMAVA) was decreased in microglia of antibiotics-treated mice. TMAVA administration diminished the activity of TLR4/p38MAPK pathway in microglia, and reversed T cell infiltration in the brain. We also found reduced TMAVA abundance in the blood of patients after GVHD onset compared to before onset. In summary, we identified the loss of bacteria-derived TMAVA upon antibiotics treatment as a central causative factor for CNS-aGVHD.
2025-06-01 | GSE279739 | GEO
Project description:Female genital tract (FGT) diseases such as bacterial vaginosis (BV) and sexually transmitted infections are prevalent in South Africa, with young women being at an increased risk. Since imbalances in the FGT microbiome are associated with FGT diseases, it is vital to investigate the factors that influence FGT health. The mycobiome plays an important role in regulating mucosal health, especially when the bacterial component is disturbed. However, we have a limited understanding of the FGT mycobiome since many studies have focused on bacterial communities and have neglected low abundance taxonomic groups, such as fungi. To reduce this knowledge deficit, we present the first large-scale metaproteomic study to define the taxonomic composition and potential functional processes of the FGT mycobiome in South African reproductive-age women. We examined FGT fungal communities present in 123 women by collecting lateral vaginal wall swabs for liquid chromatography-tandem mass spectrometry.
2025-03-28 | PXD046053 | Pride
Project description:We investigated the differences in paneth cell gene expression in different intestinal microbiome contexts and with and without zinc supplementation. We used mice housed in an SPF animal house that wre untreated, mice housed in ans SPF animal house that were treated with antobiotics for 3 weeks and germ-free mice to investigated the effect of the microbiome on paneth cell gene expression. Zinc is an essential element for paneth cell fuction. Mice of each group were further divide in zinc supplemented and non-zinc supplemented drinking water subgroups. This allowed us to check if zinc would enhance the differences between SPF, atibioicts and germ-free mice or reduce them.
2025-02-26 | GSE281682 | GEO
Project description:DNA methylation is an epigenetic mark that is altered in cancer and aging tissues. The effects of extrinsic factors on DNA methylation remain incompletely understood. Microbial dysbiosis is a hallmark of colorectal cancer, and infections have been linked to aberrant DNA methylation in cancers of the GI tract. To determine the microbiota’s impact on DNA methylation, we studied the DNA methylation of colorectal mucosa in germ-free (GF, no microbiome) and specific pathogen free (SPF, controlled microbiome) mice, as well as in interleukin 10 KO mice (Il10-/-) which are prone to inflammation and tumorigenesis in the presence of a microbiome. We compared DNA methylation changes to those seen in aging, and after exposure to the colon carcinogen azoxymethane (AOM). DNA methylation changes associated with aging were accelerated in the Il10-/- /SPF mice. By contrast, AOM induced profound hypomethylation that was distinct from the effects of aging or of the microbiome. CpG sites modified by the microbiome were over-represented among DNA methylation changes in colorectal cancer. Thus, the microbiome affects the DNA methylome of colorectal mucosa in patterns reminiscent of what is observed in colorectal cancer.
2023-05-09 | GSE150333 | GEO
Project description:Mature blood cells are maintained throughout life by hematopoietic stem cells (HSC). With aging, both HSC self-renewal as well as multi-lineage differentiation fidelity decline, a process determined by cell-intrinsic and –extrinsic factors. We here studied which aging-associated bone marrow (BM) alterations contribute to this process. Aged specific pathogen free (SPF) WT mice have increased systemic levels of microbial compounds compared to their young counterparts. This associates with increased steady-state IL-1a/b production by multiple BM cell populations. Aging-associated inflammatory transcriptional signatures and functional myeloid-differentiation bias in HSCs were mitigated in aged IL-1R1KO SPF and WT germ-free mice. Moreover, myeloid cells from aged mice produce more IL-1b and aged mice show higher and more durable IL-1a/b increase to lipopolysaccharide (LPS) challenges. Reducing inflammatory burden in aged mice by inhibiting IL-1 signaling or by antibiotic treatment rejuvenate HSCs functions. Collectively we define the microbiome-IL-1-IL1R1 axis as a key driver of HSC aging.
2021-09-16 | GSE163503 | GEO
Project description:Interventions: Group 1: Arm 1 - colon cancer
-> 16sRNA microbiome analysis (stool at time of initial diagnosis/ stool post operative/ stool during follow up; healthy normal tissue of the proximal and distal resection margin; tumor tissue)
Group 2: Arm 2 - rectal cancer
-> 16sRNA microbiome analysis (stool examination at time of initial diagnosis/ if neoad. therapy than stool examination after completion of neoadj. therapy/ stool examination post operative and during follow up; healthy normal tissue of the proximal and distal resection margin; tumor tissue)
Primary outcome(s): 16sRNA analysis of the microbiome (stool at initial diagnosis and postoperatively at primary surgery, or before neoadj. therapy and after completion, tumor tissue intraoperatively) in patients with CRC.
Study Design: Allocation: ; Masking: ; Control: ; Assignment: ; Study design purpose: other
| 2439238 | ecrin-mdr-crc
Project description:TH2 and innate lymphoid cells 2 (ILC2) can stimulate tumor growth by secreting pro-tumorigenic cytokines such as IL4, IL5 and IL13. However, the mechanisms by which type 2 immune cells traffic to the tumor microenvironment (TME) are unknown. Here, in pancreatic ductal adenocarcinoma (PDAC), we show that oncogenic KrasG12D (Kras*) increases the expression of IL33 in cancer cells, which upon secretion recruits and activates the TH2 and ILC2. Correspondingly, cancer cell-specific deletion of IL33 reduces TH2 and ILC2 recruitment and promotes tumor regression. Unexpectedly, we discovered that the cellular release of IL33 into the TME is dependent on the intratumoral fungal mycobiome. Genetic deletion of IL33 or anti-fungal treatment decreases TH2 and ILC2 infiltration and increases survival. Consistent with these murine data, high IL33 expression is observed in approximately 20% of human PDAC, and expression is mainly restricted to cancer cells. These data expand our knowledge of the mechanisms driving PDAC tumor progression and identifies therapeutically targetable pathways involving intratumoral mycobiome-driven secretion of IL33.
2022-03-01 | GSE190103 | GEO
Project description:Aging is associated with declining immunity and inflammation as well as alterations in the gut microbiome with a decrease of beneficial microbes and increase in pathogenic ones. The aim of this study was to investigate aging associated gut microbiome in relation to immunologic and metabolic profile in a non-human primate (NHP) model. 12 old (age>18 years) and 4 young (age 3-6 years) Rhesus macaques were included in this study. Immune cell subsets were characterized in PBMC by flow cytometry and plasma cytokines levels were determined by bead based multiplex cytokine analysis. Stool samples were collected by ileal loop and investigated for microbiome analysis by shotgun metagenomics. Serum, gut microbial lysate and microbe-free fecal extract were subjected to metabolomic analysis by mass-spectrometry. Our results showed that the old animals exhibited higher inflammatory biomarkers in plasma and lower CD4 T cells with altered distribution of naïve and memory T cell maturation subsets. The gut microbiome in old animals had higher abundance of Archaeal and Proteobacterial species and lower Firmicutes than the young. Significant enrichment of metabolites that contribute to inflammatory and cytotoxic pathways was observed in serum and feces of old animals compared to the young. We conclude that aging NHP undergo immunosenescence and age associated alterations in the gut microbiome that has a distinct metabolic profile.
2022-02-01 | E-MTAB-10160 | biostudies-arrayexpress
Project description:We report the RNAseq of mouse pancreatic cancer cell lines with Kras ON vs Kras OFF. TH2 and innate lymphoid cells 2 (ILC2) can stimulate tumor growth by secreting pro-tumorigenic cytokines such as IL4, IL5 and IL13. However, the mechanisms by which type 2 immune cells traffic to the tumor microenvironment (TME) are unknown. Here, in pancreatic ductal adenocarcinoma (PDAC), we show that oncogenic KrasG12D (Kras*) increases the expression of IL33 in cancer cells, which upon secretion recruits and activates the TH2 and ILC2. Correspondingly, cancer cell-specific deletion of IL33 reduces TH2 and ILC2 recruitment and promotes tumor regression. Unexpectedly, we discovered that the cellular release of IL33 into the TME is dependent on the intratumoral fungal mycobiome. Genetic deletion of IL33 or anti-fungal treatment decreases TH2 and ILC2 infiltration and increases survival. Consistent with these murine data, high IL33 expression is observed in approximately 20% of human PDAC, and expression is mainly restricted to cancer cells. These data expand our knowledge of the mechanisms driving PDAC tumor progression and identifies therapeutically targetable pathways involving intratumoral mycobiome-driven secretion of IL33.
2022-03-01 | GSE190468 | GEO
Project description:SPF Mice were transplanted with wildling microbiota and characterized regarding microbiome composition and immune functionality
| PRJEB84922 | ENA