Project description:To better understand the impact of infection on oocyte quality we employed global transcriptomics of oocytes collected from heifers after receiving intrauterine infusion of pathogenic Escherichia coli and Trueperella pyogenes. We hypothesized that oocyte transcriptome would be altered in response to intrauterine infection. A total of 452 differentially expressed genes were identified in oocytes collected from heifers 4 days after bacteria infusion compared to vehicle infusion, while 539 differentially expressed genes were identified in oocytes collected from heifers 60 days after bacteria infusion. Only 42 genes were differentially expressed in bacteria infused heifers at both day 4 and day 60. Interferon, HMGB1, ILK, IL-6 and TGF-beta signaling pathways were downregulated in oocytes collected at day 4 from bacteria infused heifers, while interferon, ILK and IL-6 signaling were upregulated in oocytes collected at day 60 from bacteria infused heifers. These data suggest that bacterial infusion alters the oocyte transcriptome differently at day 4 and day 60, suggesting different follicle stages are susceptible to damage. Characterizing the long-term impacts of uterine infection on oocyte transcriptome aids in our understanding of how infection causes infertility in dairy cattle.
Project description:Transcriptional profiling of Caco-2 cells co-cultured with Faecalibacterium prausnitzii DSM17677, Lactobacilus rhamnosus HN001, UV-killed F. prausnitzii, or no bacteria in an apical anaerobic environment for four hours.
Project description:In order to get insights into the ability of ectomycorrhizal fungi to perceive their biotic environment as well as into the mechanisms of the interactions between ectomycorrhizal fungi and soil bacteria, we analysed the transcriptomic response of the ectomycorrhizal fungus L. bicolor and of two beneficial, and neutral soil bacteria during their interactions in vitro.
Project description:Transcriptional profiling of Caco-2 cells co-cultured with Faecalibacterium prausnitzii DSM17677, Lactobacilus rhamnosus HN001, UV-killed F. prausnitzii, or no bacteria in an apical anaerobic environment for four hours. 2 colour microarray, reference design. Biological replicates: 6 per treatment group.
Project description:The aim of this experiment was to determine if the development of resistance to antibiotics can be driven by the concentration and speciation of Cu. Experimental setup was designed to investigate two hypotheses for which two strains of Gram- bacteria have been selected: - Do TE enhance AR in resistant bacteria? Resistant strain: Bioluminescent Pseudomonas aeruginosa PAO1 (Xen41, Tetracycline resistant) - Do TE induce AR in sensitive bacteria? Sensitive strain: Pseudomonas aeruginosa PAO1 (Wild Type)
Project description:Nicotinamide adenine dinucleotide (NAD), a cofactor for hundreds of metabolic reactions in all cell types, plays an essential role in diverse cellular processes including metabolism, DNA repair, and aging. NAD metabolism is critical to maintain cellular homeostasis in response to environmental signals, however, how it is impacted by the environment remains unclear. Here, we report an unexpected trans-kingdom cooperation between bacteria and mammalian cells wherein bacteria contribute to host NAD biosynthesis. Bacteria confer mammalian cells with the resistance to inhibitors of NAMPT, the rate limiting enzyme in the main vertebrate NAD salvage pathway. Mechanistically, a microbial nicotinamidase (PncA) that converts nicotinamide to nicotinic acid, a key precursor in the alternative deamidated NAD salvage pathway, is necessary and sufficient for this protective effect. This bacteria-enabled bypass of the pharmacologically induced metabolic block in mammalian cells represents a novel paradigm in drug resistance. This host-microbe metabolic interaction also dramatically enhances the hepatic NAD-boosting efficiency of nicotinamide and nicotinamide riboside supplementation, demonstrating a crucial role of microbes, gut microbiota in particular, in systemic NAD metabolism.
