Sickness Behavior and the Metabolic Demand of Immunity: Insight from a Live Bacterial Infection Model.
Type of DegreePhD Dissertation
Restriction TypeAuburn University Users
MetadataShow full item record
Life-history theory states that animals have access to a finite amount of resources over their lifespan. These resources are allocated between growth, reproduction, and maintenance, and how these resources are allocated will affect the overall fitness of an organism. A fundamental assumption of this theory is that once a resource is utilized by a trait, it cannot be used by another trait. Thus, when the demand for resources for one trait increases, it will come at the cost of the other traits. The host’s immune system is responsible for survival from pathogenic invasions. Therefore, it is a critical part of maintenance. Studies have examined the trade-offs induced by an immune response. The current knowledge on trade-offs incurred during an immune response come from the use of pathogen-associated molecular patterns (PAMPs), non-pathogenic antigens such as sheep red blood cells (SRBCs), or keyhole limpet hemocyanin (KLH). These studies have observed trade-offs with metabolism and weight. Additionally, some of these studies have observed decreased activity, increased fatigue, loss of appetite, and fever. Collectively, these symptoms are knowns as sickness behavior. In recent years, the field of science investigating the cellular metabolism of immune cells termed immunometabolism has observed a rapid growth. However, the knowledge gained from these studies relies on PAMPs or non-specific activation of cells of the adaptive immune system. Thus, the understanding of trade-offs and immunometabolism to a pathogen remains poorly characterized. Our present study aims to longitudinally characterize the trade-off to life-history traits, induced sickness behavior, and immunometabolism to a well-characterized model Listeria monocytogenes. During a primary immune response, we observed trade-offs and sickness behavior that corresponded to the timing of the innate immune response. Additionally, during this time, we observed a shift in cellular metabolism towards aerobic glycolysis in cells of the innate immune system. During the time of maximal cost of adaptive immunity, clonal expansion, we observed the resolution trade-offs and sickness behavior. Additionally, the cell’s immunometabolism resembled cells from control. Thus, during a primary immune response, the innate immune system likely is the driver of trade-offs. During a secondary response, we observed trade-offs that coincided with the timing of reactivation of cells of the adaptive immune system. Thus, reactivation of the adaptive immune response is likely to cause trade-offs.