Immune Responses Accelerate Ageing: Proof-of-Principle in an Insect Model

The pathology of many of the world's most important infectious diseases is caused by the immune response. Additionally age-related disease is often attributed to inflammatory responses. Consequently a reduction in infections and hence inflammation early in life has been hypothesized to explain the rise in lifespan in industrialized societies. Here we demonstrate experimentally for the first time that eliciting an immune response early in life accelerates ageing. We use the beetle Tenebrio molitor as an inflammation model. We provide a proof of principle for the effects of early infection on morbidity late in life and demonstrate a long-lasting cost of immunopathology. Along with presenting a proof-of-principle study, we discuss a mechanism for the apparently counter-adaptive persistence of immunopathology in natural populations. If immunopathology from early immune response only becomes costly later in life, natural selection on reducing self-harm would be relaxed, which could explain the presence of immune self-harm in nature.

全球诸多重大传染性疾病的病理损伤均由免疫应答介导。此外，年龄相关性疾病通常也与炎症应答密切相关。因此，有假说提出，生命早期感染及随之而来的炎症反应的减少，可用于解释工业化社会人类寿命的延长。本研究首次通过实验证实，生命早期触发免疫应答会加速衰老进程。本研究以黄粉虫（Tenebrio molitor）作为炎症模型，验证了生命早期感染对晚年发病的影响，并证实了免疫病理存在长期代价。作为一项原理验证性研究，我们同时探讨了自然种群中免疫病理为何会以看似反适应性的方式持续存在的机制：若早期免疫应答引发的免疫病理仅在生命后期才产生代价，那么针对减少自身损伤的自然选择便会放松，这或可解释自然界中免疫自身损伤现象的存在。