Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1137132 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29872651_1.fastq.gz | Fastqsanger.gz | |||
| SRR29872651_2.fastq.gz | Fastqsanger.gz | |||
| SRR29872652_1.fastq.gz | Fastqsanger.gz | |||
| SRR29872652_2.fastq.gz | Fastqsanger.gz | |||
| SRR29872653_1.fastq.gz | Fastqsanger.gz |
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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:Abstract: Many mouse models of neurological disease use the tetracycline transactivator (tTA) system to control transgene expression by oral treatment with the broad-spectrum antibiotic doxycycline. Antibiotic treatment used for transgene control might have undesirable systemic effects, including the potential to affect immune responses in the brain via changes in the gut microbiome. Recent work has shown that an antibiotic cocktail to perturb the gut microbiome can suppress microglial reactivity to brain amyloidosis in transgenic mouse models of Alzheimer's disease based on controlled overexpression of the amyloid precursor protein (APP). Here we assessed the impact of chronic low dose doxycycline on gut microbiome diversity and neuroimmune response to systemic LPS challenge in a tTA-regulated model of Alzheimer's amyloidosis. We show that doxycycline decreased microbiome diversity in both APP transgenic and wild-type mice and that these changes persisted long after drug withdrawal. Despite this change in microbiome composition, dox treatment had minimal effect on transcriptional signatures in the brain, both at baseline and following acute LPS challenge. Our findings suggest that central neuroinflammatory responses may be less affected by dox at doses needed for transgene control than by antibiotic cocktail at doses used for microbiome manipulation.
2024-01-10 | GSE236242 | GEO
Project description:Transcriptional profiling of the microdissected SVZ from 7-month-old mice Adult neurogenesis is suppressed in the SVZ of 3xTg mice, a model of Alzheimer's disease. To better understand the underlying mechanisms of this suppression, the goals of this experiment were to compare the transcriptional profiles of the SVZ neural stem cell niche in 3xTg-AD mice versus strain controls. We used early middle-aged mice (7-months-old) rather than old mice, in order to identify genetic changes that are not caused secondarily to other degenerative changes occurring in these mice. Two-condition experiment, 3xTg vs WT SVZ. Biological replicates: 4 for each.
2015-08-01 | E-GEOD-60460 | biostudies-arrayexpress
Project description:In this study, we investigated the therapeutic potential of a well-tolerated immunomodulatory relapsing-remitting multiple sclerosis drug, glatiramer acetate (GA), on the 3xTg mouse model of Alzheimer's Disease. Briefly, we treated aged female 3xTg mice (>15 mo) weekly with 0.1 mg of GA for 8 weeks. We were able to observe an improvement in cognition and amelioration of amyloid pathology, which we attempted to correlate with changes in microglial transcriptome. To this end, we sorted microglia (CD45int CD11b+) from the hippocampi of GA or PBS-treated 3xTg mice for bulk RNA-seq.
2021-08-27 | GSE169216 | GEO
Project description:Transcriptional profiling of the microdissected SVZ from 7-month-old mice Adult neurogenesis is suppressed in the SVZ of 3xTg mice, a model of Alzheimer's disease. To better understand the underlying mechanisms of this suppression, the goals of this experiment were to compare the transcriptional profiles of the SVZ neural stem cell niche in 3xTg-AD mice versus strain controls. We used early middle-aged mice (7-months-old) rather than old mice, in order to identify genetic changes that are not caused secondarily to other degenerative changes occurring in these mice.
2015-08-01 | GSE60460 | GEO
Project description:In this study, we aimed to deplete the aging microglia and investigate the impact of the newly-born microglia in Alzheimer's pathology using the 3xTg mouse model. Specifically, >24 mo male 3xTg mice were given chow containing 1200mg/kg PLX5622 (AIN-76A-D1001i, Research Diests, NJ, USA) for 2 weeks to deplete their microglia. Control diet with the same base formula were given to control group and to experimental groups during a 4-week repopulation phase immediately following PLX treatment. At the end of the repopulation, we pooled sorted, viable microglia (CD45int CD11b) from 3-5 mice/group and ran single-cell RNAseq analysis to determine the similarities and differences between the aged and repopulated cells in the context of Alzheimer's Disease. We also included non-transgenic controls as a separate group.
2022-02-01 | GSE190607 | GEO
Project description:The goals of this study are to compare transcriptome profiling (RNA-seq) in wild-type (NTG) and 3xTg-AD mice, to determine the transcriptomal changes of neural stem and progenitor cells (NSPC) from the SGZ at early stages of Alzheimer's Disease in a mouse model. Methods: A tamoxifen (TAM)-inducible Nestin-CreERT2;ROSA26-EYFP reporter mouse line was cross-bred with NTG or 3xTG-AD mice to label NSPC upon TAM administration. YFP-positive NSPCs were sorted through FACS (Fluorescence-Activated Cell Sorting) 10 days after TAM from NTG; Nestin-CreERT2;ROSA26-EYFP and 3xTg-AD;Nestin-CreERT2;ROSA26-EYFP mice. RNA was extracted with RNeasy Micro Kit and deep-sequenced on the NovaSeq SP flowcell SR200 platform. The sequence reads of Fastq files that passed quality filters were aligned to the mouse genome (build mm10) using hisat2. Samtools was used to index the BAM files. DESeq2 was used to establish differential gene expression between NTG and 3xTg-AD samples. Results: We mapped about 48 million sequence reads per sample to the mouse genome (build mm10) and identified 1391 genes that were differentially expressed in the 3xTg-AD, with 720 down- and 671 up-regulated. Genes were considered significantly different between two genotypes if they meet the following criteria: 1) adjusted p-value < 0.05, and 2) log2 fold change > 0.5 or < -0.5. Conclusions: Gene ontology analysis of differentially expressed genes uncovered several pathways that may contribute to early neural stem cell decline in the 3xTg mice. Our results revealed very early perturbations in the SGZ neurogenic niche in the 3xTg mouse model of AD, manifested by intrinsic molecular changes in neural stem and progenitor cells (NSPC) at juvenile age, resulting in dysregulated neural stem cell homeostasis.
2023-02-15 | GSE218323 | GEO
Project description:It is well-established that women are disproportionately affected by Alzheimer’s disease (AD). The mechanisms underlying this sex-specific disparity are not fully understood, but several factors that are often associated-including interactions of sex hormones, genetic factors, and the gut microbiome-likely contribute to the disease's etiology. Here, we have examined the role of sex hormones and the gut microbiome in mediating A amyloidosis and neuroinflammation in APPPS1-21 mice. We report that postnatal gut microbiome perturbation in female APPPS1-21 mice leads to an elevation in levels of circulating estradiol. Early stage ovariectomy (OVX) leads to a reduction of plasma estradiol that is correlated with a significant alteration of gut microbiome composition and reduction in A pathology. On the other hand, supplementation of OVX-treated animals with estradiol restores A burden and influences gut microbiome composition. The reduction of A pathology with OVX is paralleled by diminished levels of plaque-associated MGnD-type microglia while estradiol supplementation of OVX-treated animals leads to a restoration of activated microglia around plaques. In summary, our investigation elucidates the complex interplay between sex-specific hormonal modulations, gut microbiome dynamics, metabolic perturbations, and microglial functionality in the pathogenesis of Alzheimer's disease.
2024-02-08 | GSE245831 | GEO
Project description:The gut microbiome is significantly altered in inflammatory bowel diseases, but the basis of these changes is not well understood. We have combined metagenomic and metatranscriptomic profiling of the gut microbiome to assess changes to both bacterial community structure and transcriptional activity in a mouse model of colitis. Gene families involved in microbial resistance to oxidative stress, including Dps/ferritin, Fe-dependent peroxidase and glutathione S-transferase, were transcriptionally up-regulated in colitis, implicating a role for increased oxygen tension in gut microbiota modulation. Transcriptional profiling of the host gut tissue and host RNA in the gut lumen revealed a marked increase in the transcription of genes with an activated macrophage and granulocyte signature, suggesting the involvement of these cell types in influencing microbial gene expression. Down-regulation of host glycosylation genes further supports a role for inflammation-driven changes to the gut niche that may impact the microbiome. We propose that members of the bacterial community react to inflammation-associated increased oxygen tension by inducing genes involved in oxidative stress resistance. Furthermore, correlated transcriptional responses between host glycosylation and bacterial glycan utilisation support a role for altered usage of host-derived carbohydrates in colitis. Complementary transcription profiling data from the mouse hosts have also been deposited at ArrayExpress under accession number E-MTAB-3590 ( http://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-3590/ ).
2015-05-22 | E-MTAB-3562 | biostudies-arrayexpress