Douhard Frédéric, Moreno-Romieux Carole, Doeschl-Wilson Andrea B
GenPhySE, Université de Toulouse, INRAE, ENVT, Castanet-Tolosan, F-31326, France.
The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, UK.
BMC Ecol Evol. 2025 Jan 28;25(1):14. doi: 10.1186/s12862-024-02340-0.
In infected hosts, immune responses trigger a systemic energy reallocation away from energy storage and growth, to fuel a costly defense program. The exact energy costs of immune defense are however unknown in general. Life history theory predicts that such costs underpin trade-offs between host disease resistance and other fitness related traits, yet this has been seldom assessed. Here we investigate immune energy cost induced by infection, and their potential link to a trade-off between host resistance and fat storage that we previously exposed in sheep divergently selected for resistance to a pathogenic helminth.
To this purpose, we developed a mathematical model of host-parasite interaction featuring individual changes in energy allocation over the course of infection. The model was fitted to data from an experimental infectious challenge in sheep from genetically resistant and susceptible lines to infer the magnitude of immune energy costs. A relatively small and transient immune energy cost in early infection best explained within-individual changes in growth, energy storage and parasite burden. Among individuals, predicted responses assuming this positive energy cost conformed to the observed trade-off between resistance and storage, whereas a cost-free scenario incorrectly predicted no trade-off.
Our mechanistic model fitting to experimental data provides novel insights into the link between energy costs and reallocation due to induced resistance within-individual, and trade-offs among individuals of selected lines. These will be useful to better understand the exact role of energy allocation in the evolution of host defenses, and for predicting the emergence of trade-offs in genetic selection.
在受感染的宿主体内，免疫反应会引发全身能量重新分配，从能量储存和生长转向为代价高昂的防御程序提供能量。然而，免疫防御的确切能量消耗总体上尚不清楚。生活史理论预测，这种消耗是宿主抗病性与其他适应性相关性状之间权衡的基础，但这一点很少得到评估。在此，我们研究感染引起的免疫能量消耗，以及它们与宿主抗性和脂肪储存之间权衡的潜在联系，我们之前在对致病性蠕虫具有不同抗性的绵羊中揭示了这种权衡关系。
为此，我们建立了一个宿主 - 寄生虫相互作用的数学模型，该模型描述了感染过程中能量分配的个体变化。该模型与来自具有遗传抗性和易感性品系的绵羊实验性感染挑战的数据相拟合，以推断免疫能量消耗的大小。早期感染中相对较小且短暂的免疫能量消耗最能解释个体内部生长、能量储存和寄生虫负担的变化。在个体之间，假设这种正能量消耗的预测反应符合观察到的抗性与储存之间的权衡，而无消耗的情况错误地预测不存在权衡。
我们的机制模型与实验数据拟合，为个体内部因诱导抗性导致的能量消耗和重新分配之间的联系，以及所选品系个体之间的权衡提供了新的见解。这些将有助于更好地理解能量分配在宿主防御进化中的确切作用，以及预测遗传选择中权衡的出现。
