Tradeoffs among immune function, metabolic rates and other ecological traits.
AuthorDowns, Cynthia Joy
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Life histories generally fall on a continuum of slow-to-fast paced. Fast-paced life histories are characterized by shorter lifespan, lower survival, higher reproductive rate, and faster development, and slow-paced life histories are characterized by the opposite traits. The life history-physiology nexus proposes that physiological mechanisms - specifically metabolic rates, immune function, and endocrine hormones - mediate life history tradeoffs and can explain this general pattern. This dissertation addresses three aspects of the life history-physiology nexus.First, I investigated how metabolic rate scales with body mass and body temperature in animals and plants. Recent work has questioned (1) whether there is a universal scaling exponent for body mass and (2) how temperature affect metabolic rates. I tested the Arrhenius fractal supply model (AFS), the basis for the metabolic theory of ecology. That theory assumes that the scaling exponent for body mass is 3/4. Originally, it also assumed that metabolic responses to body temperature, measured as activation energies, should fall between 0.2 to 1.2 eV. Later, this prediction was revised and narrowed to 0.6 and 0.7 eV. I used multiple regressions of ln(metabolic rate) as a function of ln(body mass) and 1/(body temperature) to fit the best scaling exponent for body mass to nine datasets of many diverse species. For the majority of the datasets, in addition to not supporting a scaling exponent of 3/4, the analyses indicated that effects of body temperature sometimes fell outside the range of 0.6 to 0.7 eV. My analyses demonstrate that the AFS model does not hold universally.Second, I investigated how artificial selection on metabolic rates affects immune function. The pace-of-life theory posits that fast-paced individuals with have high basal metabolic rates (BMR), high maximal metabolic rates (MMR), and reduced immune function. With respect to BMR this is often assumed in the literature, but previous work has not looked carefully at immune associations with MMR. In addition, because basal metabolic rate and maximal metabolic rate are often correlated, without careful experiment design their effects might easily be conflated. I used lines of mice selected for high maximal metabolic rates to test how selection on metabolic rate alters immune function. After measuring maximal and basal metabolic rates, I challenged these mice with lipopolysaccharide (LPS) and quantified circulating cytokines using luminex technologies to assess inflammatory response. I also immunized mice from these lines with keyhole limpet hemocyanin and quantified circulating antibodies using ELISAs to assess humoral immune capabilities. Selection on maximal metabolic rate, but not on basal metabolic rate, inhibited both innate and adaptive immune function. These results suggests that physiologists and ecologists looking for tradeoffs with metabolic rates, should shift their attention to studying tradeoffs with MMR rather than focusing on tradeoffs with BMR.Third, I investigated immune function in mice selected for high voluntary wheel running. Immune function is an important component of Darwinian fitness. Signaling molecules, such as corticosterone, that affect both immune function and energy metabolism may cause tradeoffs with other aspects of the life history - physiology nexus. To test the hypothesis that an evolved increase in corticosterone will suppress immune function I used mice selected for high voluntary wheel running (HR lines). These mice circulating baseline corticosterone that is twice that of mice from randomly bred, control lines (C lines). I injected female mice with LPS. Compared to C mice, the inflammatory response of HR mice was not suppressed. Thus, it appears that selection for high voluntary wheel running did not alter immune function. My results suggest that effects of evolutionary derived differences in baseline corticosterone levels may be very different from effects caused by environmental factors that alter baseline corticosterone levels during the course of an individual animal's life. Consequently, evolved increases in stress hormones may not lead to the detrimental suppression of the inflammatory response associated with chronic increases in stress hormones.