Schiavinato Matteo, Ronanki Shivani, Estruch Ignacio Miro, van den Brink Nico
Cluster of Biomolecular Science, Division of Toxicology, Wageningen University and Research, 6708 WE Wageningen, The Netherlands.
Biol Lett. 2025 Jan;21(1):20240618. doi: 10.1098/rsbl.2024.0618. Epub 2025 Jan 22.
Dealing with infections is a daily challenge for wild animals. Empirical data show an increase in reactive oxygen species (ROS) production during immune response. This could have consequences on telomere length, the end parts of linear chromosomes, commonly used as proxy for good health and ageing. Telomere length dynamics may reflect the costs associated with physiological responses. In this study, immune system of blue tit () nestlings was experimentally challenged through a polyinosinic:polycytidylic acid (poly I:C) injection, a synthetic double-stranded RNA that mimics a virus, activating the pathway of immune response triggered via the toll-like receptors 3. This path is known to form ROS downstream. Immune response was quantified by white cell counts in blood, while brain lipoperoxidation has been evaluated as an indicator of oxidative damage. Finally, individuals' telomere length shortening between days 8 and 15 after hatching was measured in erythrocytes. Challenged nestlings showed increased leukocyte number when compared with control (treated with a saline solution), lower brain lipid peroxidation (likely as a result of a compensatory mechanism after oxidative stress burst) and accelerated telomere shortening. These findings support the 'ageing cost of infections pathway' hypothesis, which supposes a role for infections in quick biological ageing.
应对感染是野生动物每天都面临的挑战。实证数据表明,免疫反应过程中活性氧(ROS)的产生会增加。这可能会对端粒长度产生影响,端粒是线性染色体的末端部分,通常被用作健康和衰老状况的指标。端粒长度动态变化可能反映了与生理反应相关的代价。在本研究中,通过注射聚肌苷酸:聚胞苷酸(poly I:C)对蓝山雀雏鸟的免疫系统进行实验性刺激,poly I:C是一种模拟病毒的合成双链RNA,可激活通过Toll样受体3触发的免疫反应途径。已知该途径会在下游形成ROS。通过血液中的白细胞计数来量化免疫反应,同时将脑脂质过氧化作为氧化损伤的指标进行评估。最后,测量雏鸟孵化后第8天到第15天红细胞中端粒长度的缩短情况。与对照组(用盐溶液处理)相比,受到刺激的雏鸟白细胞数量增加,脑脂质过氧化程度较低(可能是氧化应激爆发后补偿机制的结果),端粒缩短加速。这些发现支持了“感染的衰老成本途径”假说,该假说认为感染在快速生物衰老过程中起作用。