349 - Awardee Talk: How the Immune System Interacts with Ruminant Nutrient Partitioning

Adverse weather conditions are a large constraint to maximizing farm animal productivity. Heat stress, in particular, compromises almost every metric of animal agriculture profitability. Suboptimal production during HS was traditionally thought to result from hypophagia. However, independent of inadequate nutrient consumption, HS affects a plethora of endocrine, physiological, metabolic, circulatory, and immunological variables. Mounting evidence suggest that direct effects of HS originating at the gastrointestinal tract precede the observed effects on the aforementioned systems. Heat stress compromises intestinal barrier integrity causing the appearance of luminal contents, e.g. endotoxin, in circulation. Endotoxin stimulates both a classic immune response with local and systemic inflammatory reactions as well as directly acting on numerous organs and tissues. Once activated, leukocytes switch from oxidative phosphorylation to aerobic glycolysis where the glucose requirement of an intensely triggered immune system can exceed 2 kg/d in a lactating dairy cow. Whole body metabolic adjustments are primarily characterized by increased basal and stimulated circulating insulin, increased hepatic glucose output, decreased adipose tissue mobilization, and decreased skeletal muscle flexibility characterized by a reliance on glucose as a fuel substrate rather than lipid. Ultimately, the metabolic and physiological consequences of heat stress share a similar phenotype with immune challenges. Describing the physiology and mechanisms that underpin how HS jeopardizes animal performance is critical for developing approaches to ameliorate current production issues and requisite for generating future strategies (genetic, managerial, nutritional, and pharmaceutical) aimed at optimizing animal well-being, and improving the sustainable production of high-quality protein for human consumption.