A nutrient deficit develops immediately postpartum when dairy cows drop in feed intake but metabolic demands of milk production have to be filled. Cows express a heightened inflammatory response and inefficient pathogen clearance during this time. This immune dysfunction, associated with the time of metabolic challenge, is more severe in animals with the greatest nutrient deficit. However, the mechanistic link has not been determined to date. This hampers our ability to address the cause of poor immune function and damaging inflammation after calving when cows are at the highest risk for developing infectious diseases. Our global hypothesis is that the nutrient deficit is detected by immune cells through nutrient-sensing kinases, which in turn orchestrate immune cell phenotype, and shift the inflammatory response to a pro-inflammatory state as has been demonstrated in other mammalian species. Our objective is to describe the temporal changes in nutrient-sensing kinase signaling in the transition period of dairy cows as well as the responsiveness to stimulation. Furthermore, we will investigate if supplementation with amino acids can improve inflammatory response through nutrient-sensing kinase signaling pathways in the immediate postpartum period.