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Nutrient partitioning during intramammary inflammation: A key to severity of mastitis and risk of subsequent disease?
In early lactation, susceptibility to disease is greatest, impacting cow health, productivity and leading to economic losses. Mastitis is the most economically costly disease to the dairy industry and is most frequent at this time. Glucose and amino acids (especially glutamine) are the primary fuels used by leukocytes in other species and are essential substrates for optimal leukocyte function but has not been elucidated in bovine leukocytes. Yet, because these substrates are in high demand to support milk synthesis in early lactation, their supply to leukocytes may be compromised. Production-related metabolic diseases during early lactation, such as ketosis and hepatic lipidosis, can also adversely affect health and productivity. Risk of subsequent disease for cows during mastitis is unknown. During an inflammatory response, increases in circulating non-esterified fatty acids and glucose during an IMI in dairy cows have been reported. Previous work indicates that hepatic expression of key genes associated with gluconeogenesis (e.g. PCK1 and G6PC), ketogenesis (e.g. HMGCS2) and fatty acid metabolism (e.g. SREBF1 and PPARA) are down-regulated after intramammary infection (IMI). These results suggest a potential link between mastitis and the risk of subsequent metabolic disease for dairy cows during lactation. This presentation will discuss the complex relationships between metabolism and immune function, and how these immunometabolic interactions relate to susceptibility to mastitis and increase the risk of subsequent disease during early lactation. New strategies to prevent or control mastitis development and reduce the risk of subsequent disease during early lactation will also be discussed.
Keywords:
cow, mastitis, metabolism