Project description:Necrotizing enterocolitis (NEC) is a severe intestinal disorder connected to a gut microbiota dysbiosis. Approximately 7-8% of very low birth weight (VLBW) infants are diagnosed with NEC with mortality rates reaching 20-50%. Fecal virome transfer (FVT) is an approach where the bacteria-free fecal fraction from a healthy donor is administered to a patient with a GM dysbiosis. FVT contains e.g. bacteriophages, eukaryotic viruses, and metabolites. Oral administered FVT from healthy milk-fed term pigs shows promising potential in preventing NEC in the preterm piglet model. However, efficacy and safety are inconsistent between experiments. In the current study, we aim to explore methods of creating reproducible FVT-like treatments and test if these act preventive against NEC and possess minimal side effects in the preterm piglet model. Using cesarean-delivered, formula-fed preterm pigs, we compare the NEC preventive effect of native donor fecal virome (nFV) with: 1) a defined bacteriophage cocktail targeting NEC-associated bacteria; and 2) a chemostat fecal virome propagation with lactose as the major carbohydrate source (cFV), and 3) chemostat fecal virome propagation with lactose and milk oligosaccharides (cFV-OS). All methods will be compared to control treatment with SM buffer (SM).
Project description:The main objective of this study was to evaluate the effect of low-protein (LP) diet on adipose tissue deposition in Krškopolje pigs reared either in organic outdoor (n=2x12) or conventional indoor (n=2x12) system. In the outdoor system, RNA-sequencing revealed the upregulation of 28 genes and downregulation of 37 genes. Upregulated genes were mainly involved in lipid metabolism (ACLY, FASN, ACACA, MOGAT2), oxidative stress, and mitochondrial function. In the indoor system, RNA-sequencing revealed 30 upregulated and 28 downregulated genes. Among the upregulated genes, heat shock proteins (HSP70.2, HSPA6) were detected in pigs on LP diet, while genes involved in the innate immune system (MSR1, TREM2, CSF3R) were downregulated.
