Project description:We compared gene expression in oviduct tissues between unmated (control) and mated hen. As spermatozoa are foreign to the female reproductive tract therefore we were interested to look at how spermatozoa survive in the female reproductive tract and keep their fertilization potentiality. To check that we collected tissues from oviduct of both control and mated female chicken and compared if sperm deposition to the oviduct made any gene expression shift related to sperm survival.
Project description:The microbiome encompasses the array of microorganisms inhabiting various niches in the body and is necessary for numerous physiological processes, including normal metabolism and a functioning immune system. Not only does the absence of a microbiome in mice impact the exposed animals but also inherited phenotypes in successive generations of progeny, suggesting that the absence of a microbiome impacts the germline and gametes. Indeed, recent research has identified a role of the gut microbiome in contributing to male fertility, in both healthy and disease states. While this link is beginning to be established, the impact of the microbiome on the male reproductive tract remains understudied. Here, we utilized a germ-free mouse model to examine the influence of the absence of microbes on the male reproductive tract. In contrast to mice with an established microbiome, germ-free mice display decreased testicular weight and the prevalence of an epididymitis-like inflammation phenotype. These histopathological changes are accompanied by transcriptomic dysregulation in the reproductive tract of germ-free mice, particularly in the cauda epididymis. Moreover, such transcriptomic changes are transmitted to the next generation with high correlation of gene expression in the cauda epididymis between germ-free mice and their conventionalized (microbiome-restored) male offspring, when compared to control mice. Ultimately, our findings identify the reproductive sequalae of males without a functional microbiome and additionally in their conventionalized offspring, suggesting that the paternal microbiota is an underappreciated contributor to male reproductive function.
Project description:Breast cancer is an age-related cancer in women with two peaks, one at 50 and one at 70 years of age. Here we used two conditional genetically engineered mouse models of breast cancer risk to study mammary gland transcriptional changes that occur as female mice age from 12 to 30 months of age, paralleling aging from 58 to 85 years of age in women. The two models express either mammary epithelial cell-targeted Estrogen Receptor (ER) alpha (Esr1) or Aromatase (CYP19A1A) over-expression beginning at age 12 or 18 months of age. Both of these risk factors increase estrogen pathway signaling, either directly though the receptor or by increasing local estrogen production. The goals of the study are to determine how quickly significant transcriptional changes occur in the mammary gland following transgene induction, to determine how the transcriptome becomes modified as the mice age past reproductive senescence through old and very old life stages, and to identify similarities and differences in the transcriptomes between the two risk conditions at different ages and conditions. The first specific objective of this transcriptome-based study is to identify significantly differentially expressed genes within each model between different ages and times of transgene induction. This includes transcriptional changes induced by 1 week, 6, 12 and 18 months of transgene expression with transgene expression initiated at age 12 months as well as transcriptional changes induced by 1 week and 6 months of transgene expression initiated at age 18 months. The second specific objective is to compare the two models at different ages (12, 18, 24 and 30 months of age) and different transgene induction times (6, 12 and 18 months) to identify differentially expressed genes between the models. Comparative control mice from each model include age 18- and 24-month-old mice without transgene induction.
Project description:Citrobacter rodentium is commonly used to elucidate mucosal responses to infection in mice developing mild disease (e.g. C57BL/6), while little is known about host responses to infection in mice developing severe disease (e.g. C3H/HeN). We report that the phyla Bacteroidetes is a minor component of the tissue-associated microbiome in uninfected C3H/HeN mice. Following infection, C. rodentium rapidly and uniformly colonises the C3H/HeN colonic mucosa, which coincides with downregulation of proteins involved in the TCA cycle and oxidative phosphorylation in intestinal epithelial cells (IECs). In contrast, we observed upregulation of DNA replication and DNA damage repair processes, as well as cholesterol biogenesis, import and export, nutritional immunity, IL-22 and INFg responses, and expression of NLRP3, in IECs. Moreover, C. rodentium triggers a staggered cell proliferation response from 3 days post infection, which correlated with a higher abundance of SLC5A9 and reduced abundance of the IEC differentiation markers SLC26A3 and CA4. Uniquely, C. rodentium triggers differential secretion of gel-forming mucins, with the number of goblet cells filled with acidic and neutral mucins dramatically increasing and decreasing, respectively. Together, these results show that despite vigorous responses, C3H/HeN mice succumb to C. rodentium infection, possibly as a result of excessive and disordered mucosal responses.
Project description:Age-dependent changes of the gut-associated microbiome have been linked to increased frailty and systemic inflammation. This study found that age-associated changes of the gut microbiome of BALB/c and C57BL/6 mice could be reverted by co-housing of aged (22 months old) and adult (3 months old) mice for 30-40 days or faecal microbiota transplantation (FMT) from adult into aged mice. This was demonstrated using high-throughput sequencing of the V3-V4 hypervariable region of bacterial 16S rRNA gene isolated from faecal pellets collected from 3-4 months old adult and 22-23 months old aged mice before and after co-housing or FMT.
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.
Project description:aCGH analysis of murine transgenic liver tissues affected with HCC, hybridized with age (18 months) and sex matched C57BL/6 mice. Moreover, 18months old C57BL/6 livers were hybridized with independent 18 months old C57BL/6 livers for control. Keywords: Array comparative genomic hybridization analysis (aCGH).