16SrRNA analysis from wildtype mice that were either fed or not with low protein diets for 4 weeks
Ontology highlight
ABSTRACT: 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.
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.
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.
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 16S rRNA sequencing to identify potential microbiota changes associated with Paneth cell defect in Atg16l1 T300A mice exposed to cigarette smoking. Female mice were used at 4-5 weeks of age. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. The fecal samples from the mice were collected for 16S rRNA sequencing analysis after completing 6 weeks of 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.
Project description: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.
Project description:We randomly selected 60 patients who completed paclitaxel treatment for high-throughput sequencing. Grade 2 or higher (grade 2+) neuropathy has been defined as high-PIPN and Grade 1 as low-PIPN according to the National Cancer Institute Common Toxicity Criteria for Adverse Events (NCI-CTCAE version 4.0) and the European Organization for Research and Treatment of Cancer CIPN specific self-report questionnaire (EORTC QOL-CIPN20). We compared gut microbiome signatures in high-PIPN, low-PIPN, and healthy controls.
Project description:To address the role of gut microbiota in the development of paclitaxel-induced peripheral neuropathy (PIPN), we performed 16S rRNA sequencing analysis of feces samples at 14 days and 28 days after the initiation of paclitaxel or vehicle injections.
Project description:We found that low protein diet consumption for 3 weeks resulted in reduction in the Paneth cells and goblet cells and villous height in wild type mice, indicating that low protein diet could negatively affect gut pathology. We performed transcriptional profiling to identify dysregulated molecular pathways in wild type mice exposed to low diet. Male mice were used at 4-5 weeks of age. The full-thickness ileum of the mice were harvested for transcriptomic analysis after completing 4 weeks of low protein diet treatment.
Project description:Single cells from ML-DS sample 186-2 (bone marrow) were analysed to determine whether mutations in JAK2 and CSF2RB ocurred in the same or different cells in this patient. Single live, CD19neg, CD3neg, CD45mid and CD117 positive cells were sorted into 96-well plates on the BD Fusion with antibodies as described above. Cord blood single cells were sorted similarly to serve as a control for the single cell Sequencing.
Project description:The aim of this experiment was to investigate cellular heterogeneity of VE-Cadherin+ cells isolated from mouse E10.5 aorta-gonad-mesonephros region.