Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

16S rRNA sequencing of cecal microbiota from neonatal mice pre- and post-weaning

ABSTRACT: Neonatal mice were susceptible to cryptosporidium infection at 1- and 2-weeks of age, but were resistant to infection at 3- and 6-weeks of age. Diet and microbial changes are known to occur during the weaning transition in mice and we hypothesized that these changes in the intestinal luminal environment might influence resistance and susceptibility to cryptosporidium infection. As one part of testing this hypothesis, cecal microbiota composition was determined by 16S ribosomal RNA sequencing of DNA isolated from the cecal contents of mice at 1 week, 2 weeks, 3 weeks, and 6 weeks of age.

INSTRUMENT(S): Illumina MiSeq

ORGANISM(S): mouse gut metagenome

SUBMITTER: Kelli VanDussen

PROVIDER: E-MTAB-9100 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

16SrRNA analysis from wildtype mice that were either fed or not with low protein diets for 4 weeks

Project description:We found that low protein diet consumption resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that low protein diet could negatively affect Paneth cell function. We performed fecal microbiota composition profiling. Male mice were used at 4-5 weeks of age. Fecal samples were collected for microbiome analysis.

2023-07-02 | E-MTAB-11277 | biostudies-arrayexpress

16S rRNA sequencing of fecal samples from wild type mice that were either exposed or not to western diet for 8 weeks

Project description:We found that western diet consumption for 8 weeks resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that western diet could negatively affect Paneth cell function. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in wild type mice exposed to western diet. Male mice were used at 4-5 weeks of age. The whole ileum of the mice were harvested for transcriptomic analysis after completing 8 weeks of western diet treatment.

2021-12-02 | E-MTAB-8334 | biostudies-arrayexpress

16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were either exposed or not to mainstream cigarette smoking for 6 weeks

2018-10-31 | E-MTAB-5717 | biostudies-arrayexpress

16S rRNA analysis from wild type mice that were either fed or not with western diet for 3 generations

Project description:We found that western diet consumption resulted in decrease in the percentage of normal Paneth cell population in wild type mice, indicating that western diet could negatively affect Paneth cell function. Subsequent generations of western diet consumption further reduced percentages of normal Paneth cell population. We performed fecal microbiota composition profiling. Male mice were used at 4-5 weeks of age. Fecal samples were collected for microbiome analysis.

2023-01-01 | E-MTAB-10995 | biostudies-arrayexpress

16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were exposed to mainstream cigarette smoking co-housed with mice from the same genotype but not exposed to cigarette smoking

Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed cohousing experiments to test if Paneth cell phenotype is horizontally transmissible as is microbiota. Atg16l1 T300A and littermate controls that were exposed to cigarette smoking were used as microbiota donors, and these donor mice were exposed to smoking for 2 weeks prior to cohousing. Separate groups of Atg16l1 T300A and littermate controls that were not exposed to cigarette smoking were used as microbiota recipients. The microbiota recipients were co-housed with microbiota donors of the same genotype for 4 weeks, during this period the donors continued to be exposed to cigarette smoking. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. At the end of the experiment, the fecal microbiota composition was analyzed by 16S rRNA sequencing.

2018-10-31 | E-MTAB-5720 | biostudies-arrayexpress

Maternal cecal microbiota transfer rescues early-life antibiotic-induced enhancement of type 1 diabetes in mice-the short term restoration

Project description:To more directly understand the mechanisms by which CMT reduced 1PAT-induced T1D development, we examined P23 ileal gene expression profile of Non-obese diabetic mice by RNAseq. There 3 treatments C, 1P and CMT, and each treatment has 4 mice.

2021-09-02 | E-MTAB-9981 | biostudies-arrayexpress

Maternal cecal microbiota transfer rescues early-life antibiotic-induced enhancement of type 1 diabetes in mice-the long term restoration

Project description:Early-life antibiotic exposure perturbs the intestinal microbiota, alters innate intestinal immunity, and accelerates type 1 diabetes development in the NOD mouse model. Here we found that maternal cecal microbiota transfer (CMT) to NOD mice with early-life antibiotic perturbation partially rescued the induced T1D acceleration. The restoration effects on the intestinal microbiome were substantial and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways. CMT also protected against perturbed cecal and serum metabolites and normalized innate and adaptive immune effectors. CMT restored patterns of ileal microRNA and histone regulation of gene expression and exon-splicing. Based on the analyses of experimental data, we propose an innate intestinal immune network involving CD44, TLR2, and Reg3g, as well as their multiple microRNA and epigenetic regulators that sense intestinal signaling by the gut microbiota. This regulation affects downstream immunological tone, leading to protection against the tissue-specific T1D injury.

2021-09-02 | E-MTAB-9982 | biostudies-arrayexpress

Expression data from Aortic Macrophages

Project description:Normal arteries contain a large population of tissue resident macrophages (MÎ¦). Their origins, as well as the mechanisms that sustain them during homeostasis and disease, however, are poorly understood. Gene expression profiling, we show, identifies arterial MÎ¦ as a distinct population among tissue MÎ¦. Ontologically, arterial MÎ¦ arise before birth, though CX3CR1-, Csf1r-, and Flt3-driven fate mapping approaches demonstrate MÎ¦ colonization occurs through successive contributions of yolk sac (YS) and conventional hematopoiesis. In adulthood, arterial MÎ¦ renewal is driven by local proliferation rather than monocyte recruitment from the blood. Proliferation sustains MÎ¦ not only during steady state conditions, but mediates their rebound after severe depletion following sepsis. Importantly, the return of arterial MÎ¦ to functional homeostasis after infection is rapid; repopulated MÎ¦ exhibit a transcriptional program similar to resting MÎ¦ and efficiently phagocytose bacteria. Collectively, our data provide a detailed framework for future studies of arterial MÎ¦ function in health and disease. Aortic macrophages (CD11bhighF4/80highCD45+MerTK+CD64+) were isolated from C57/B6 wild-type male mice aged 6-8 weeks before and 7 days after induction of sepsis by cecal puncture. 18-20 aortas were pooled per sample. Each condition contained three biological replicates.

2015-12-07 | E-GEOD-68968 | biostudies-arrayexpress

Effects of Iron Deficiency and Risperidone treatment on the rat frontal cortex

Project description:Prenatal iron deficiency (pID) has been described to increase the risk for neurodevelopmental disorders such as autism and schizophrenia; however, the precise molecular mechanisms are still unknown. Here, we utilized high throughput mass spectrometry to examine the proteomic effects of pID in adulthood on the rat frontal cortex area (FCA). In addition, the FCA proteome was examined in adulthood following risperidone treatment in adolescence to see if these effects could be prevented. We identified 1501 proteins of which 100 were significantly differentially expressed in the FCA at post-natal day 90. Pathway Analysis of proteins affected by pID revealed changes in metabolic processes, including the tricyclic acid cycle, mitochondrial dysfunction, and P13K/Akt signaling. Interestingly, most of these protein changes were not present in the adult pID offspring who received risperidone in adolescence. Behavioral testing of pID rats demonstrated social impairment and poor performance during novelty-induced exploration in pID animals in line with a abnormal neurodevelopmental phenotype. Considering the link between prenatal iron deficiency and several neurodevelopmental disorders such as autism and schizophrenia these presented results bring new perspectives to understand the role of iron in metabolic pathways and provide novel biomarkers for future studies of prenatal iron deficiency.

2018-07-05 | PXD004975 | Pride

Rhesus macaque cecal CD45+ leukocytes

Project description:10X transcriptomics + B cell V(D)J sequencing of CD45+ leukocytes

2024-04-30 | E-MTAB-13902 | biostudies-arrayexpress