Inflammation and Immune Activation during Periods of Stress in Dairy Cattle

Throughout the year, the sustainability of the dairy industry is jeopardized because of the challenges cows face during the transition to lactation, and this is further worsened during the summer months. Daily milk production losses ranging from 1.4 to 6.3 kg have been documented for cows undergoing heat stress during late gestation. Furthermore, heat stress also impairs immune response, health, and short-term and lifelong productivity. At least 50% of the farm morbidity occurs during the first 20 days after parturition increasing the risk of cow removal from the herd. Inflammation can be triggered in response to infectious (e.g. bacteria) or non-infectious agents (e.g. endogenous danger signals). The process of parturition requires the initiation of a non-infectious inflammation which is coupled with an intense oxidative stress and several others pathological and/or adaptive responses. Other drastic events around parturition, e.g. galactopoiesis, marked reduction of feed intake, and endotoxin overload, may exacerbate the parturition-initiated inflammatory process leading to a systemic inflammation. Dairy cows orchestrate an adaptive homeorhetic process inducing insulin resistance in peripheral tissues to spare glucose for the mammary gland, potentially sacrificing nutrient supply to immune cells to some degree. Hence, as insulin resistance is associated with inflammation, it is possible that endogenous inflammation is an adaptive mechanism of dairy cows to regulate partitioning of nutrients and energy balance. Although the process of parturition is initiated by an “sterile inflammation” cows with a higher degree of inflammation during the first days after parturition have greater incidence of diseases, lower milk yields, and poorer reproductive efficiency. These associations of inflammation imply a subsequent or parallel inflammation with infectious origin, where immune cells fail to resolve infection due to an apparent hypo-responsiveness during the peripartum period. An activated immune system significantly increases the demand for nutrients. Consequently, the so-called peripartum immunosuppression may be due to a limited availability of nutrients couple with an exhausted immune system due to an aberrant sterile inflammation occurring not only in the uterus, but also in the adipose tissue, muscle, and liver. Therefore, the development of assertive nutritional strategies to optimize the extent and resolution of postpartum inflammation may improve the health and productivity of cows transitioning to lactation. However, such strategies require greater knowledge of mechanisms underlying postpartum inflammation as well as identifying the most limiting nutrients of microbial- and tissue damage- stimulated immune cells.