Department of Zoology, Southern Illinois University, Carbondale, IL, USA.
School of Biological Sciences, Washington State University, Pullman, WA, USA.
J Anim Ecol. 2018 Jan;87(1):235-246. doi: 10.1111/1365-2656.12778. Epub 2017 Nov 22.
Ubiquitous environmental stressors are often thought to alter animal susceptibility to pathogens and contribute to disease emergence. However, duration of exposure to a stressor is likely critical, because while chronic stress is often immunosuppressive, acute stress can temporarily enhance immune function. Furthermore, host susceptibility to stress and disease often varies with ontogeny; increasing during critical developmental windows. How the duration and timing of exposure to stressors interact to shape critical windows and influence disease processes is not well tested. We used ranavirus and larval amphibians as a model system to investigate how physiological stress and pathogenic infection shape development and disease dynamics in vertebrates. Based on a resource allocation model, we designed experiments to test how exposure to stressors may induce resource trade-offs that shape critical windows and disease processes because the neuroendocrine stress axis coordinates developmental remodelling, immune function and energy allocation in larval amphibians. We used wood frog larvae (Lithobates sylvaticus) to investigate how chronic and acute exposure to corticosterone, the dominant amphibian glucocorticoid hormone, mediates development and immune function via splenocyte immunohistochemistry analysis in association with ranavirus infection. Corticosterone treatments affected immune function, as both chronic and acute exposure suppressed splenocyte proliferation, although viral replication rate increased only in the chronic corticosterone treatment. Time to metamorphosis and survival depended on both corticosterone treatment and infection status. In the control and chronic corticosterone treatments, ranavirus infection decreased survival and delayed metamorphosis, although chronic corticosterone exposure accelerated rate of metamorphosis in uninfected larvae. Acute corticosterone exposure accelerated metamorphosis increased survival in infected larvae. Interactions between stress exposure (via glucocorticoid actions) and infection impose resource trade-offs that shape optimal allocation between development and somatic function. As a result, critical disease windows are likely shaped by stress exposure because any conditions that induce changes in differentiation rates will alter the duration and susceptibility of organisms to stressors or disease.
普遍存在的环境应激源通常被认为会改变动物对病原体的易感性，并导致疾病的出现。然而，暴露于应激源的时间可能是至关重要的，因为慢性应激通常会抑制免疫功能，而急性应激可以暂时增强免疫功能。此外，宿主对压力和疾病的易感性通常随着个体发育而变化；在关键的发育窗口期间增加。应激源暴露的持续时间和时间如何相互作用以塑造关键窗口并影响疾病过程尚未得到充分验证。我们使用 Ranavirus 和幼虫两栖动物作为模型系统，研究生理应激和致病性感染如何塑造脊椎动物的发育和疾病动态。基于资源分配模型，我们设计了实验来测试暴露于应激源如何可能导致资源权衡，从而塑造关键窗口和疾病过程，因为神经内分泌应激轴协调发育重塑、免疫功能和能量分配在幼虫两栖动物中。我们使用林蛙幼虫（Lithobates sylvaticus）研究慢性和急性暴露于皮质酮（占主导地位的两栖类糖皮质激素）如何通过脾细胞免疫组织化学分析与 Ranavirus 感染一起介导发育和免疫功能，该分析与 Ranavirus 感染有关。皮质酮处理影响免疫功能，因为慢性和急性暴露均抑制脾细胞增殖，尽管仅在慢性皮质酮处理中病毒复制率增加。变态时间和存活率取决于皮质酮处理和感染状况。在对照和慢性皮质酮处理中， Ranavirus 感染降低了存活率并延迟了变态，尽管慢性皮质酮暴露加速了未感染幼虫的变态速度。急性皮质酮暴露加速了变态，增加了感染幼虫的存活率。应激暴露（通过糖皮质激素作用）和感染之间的相互作用导致资源权衡，从而塑造了发育和躯体功能之间的最佳分配。因此，关键的疾病窗口可能是由应激暴露塑造的，因为任何导致分化率变化的条件都会改变生物体对应激源或疾病的持续时间和易感性。
