Fueling the immune response: what’s the cost?

Abstract

Pigs kept in environments where they are exposed to a high number of pathogenic microbes have reduced feed intake and growth, even when no obvious acute illness exists. This chronic drain on production is called immunological stress. Sentinel immune cells (e.g. macrophages) ‘sense’ the diverse microbial environment by detecting pathogen-associated molecular patterns (PAMPs), which are molecules associated with groups of pathogens. The immune sentinels detect PAMPs mainly with Toll-like receptors (TLRs). Stimulation of macrophages through their TLRs leads to the synthesis and secretion of pro-inflammatory cytokines and prostaglandins, thereby initiating the inflammatory response that recruits both soluble immune molecules and circulating immune cells. Pro-inflammatory cytokines enable the immune system to communicate with other disparate physiological systems. They rearrange the animal’s metabolic priorities, resulting in re-partitioning of nutrients away from productive processes towards responses that support the immune system. Thus, the immune system, through detection of PAMPs and production of pro-inflammatory cytokines, is the critical chain link connecting the pathogenic environment to productivity. Estimates suggest that at maintenance a healthy animal uses about 0.5-2% of the body’s lysine for leukocytes, antibodies, and acute phase proteins. When mounting a robust response to an infectious pathogen the immune response is estimated to account for about 9% of the body’s lysine. Thus, the cost of immunological stress, in terms of lysine utilization, must lie somewhere on the gradient beginning at 2% (maintenance) and ending at 9% (robust immune response). Providing additional lysine in the diet does not alleviate the reduced growth caused by immunological stress because the capacity for protein accretion is inhibited. Thus, minimizing exposure to pathogenic microbes with sound environmental management practices must remain a high priority.