Meeting Abstract
The gopher tortoise (Gopherus polyphemus) is a declining keystone species of the southeastern United States Coastal Plain ecosystem. While numerous anthropogenic sources of mortality have been attributed to G. polyphemus declines, disease has been hypothesized to be a significant source of adult mortality in this species. Climate change, and specifically climatic variability, has been shown to cause negative effects on disease resistance in ectothermic vertebrates. Herein, we investigated the role that rapid temperature change has on humoral immune responses in G. polyphemus by experimentally testing the seasonal lag hypothesis. Acclimated to seasonal states of both winter and summer, we manipulated temperatures experienced by G. polyphemus to simulate short-term temperature increases and decreases, respectively. At both baseline acclimation states and temperature-altered states, we measured in vitro cellular humoral responses. Whole blood samples were collected and circulating leukocytes were isolated using a histopaque density gradient; antibody production was measured in response to negative controls as well as lipopolysaccharide (LPS) using an Enzyme-linked immuno spot assay (ELISpot). Our results indicated a strong response of G. polyphemus lymphocytes to spontaneously secrete antibody. Using this assay, we evaluated whether long-term seasonal acclimation, as well as short-term seasonal lag effects can account for changes in humoral immune responses. Data from this study indicated a lag effect in the immune response in which we did not detect a change in response as a result of the thermal manipulation. We further discuss the constraints that climatic variability may impose on ectothermic immune responses, and how this may represent one mechanism of increased disease in G. polyphemus.
