Immune Endocrine and Epigenetics Research Group, Department of Infection and Immunity, Luxembourg Institute of Health (LIH), 29 rue Henri Koch, L-4354 Esch-sur-Alzette, Luxembourg; Faculty of Science, Technology and Medicine, University of Luxembourg, 2 avenue de Université, L-4365 Esch-sur-Alzette, Luxembourg.
Immune Endocrine and Epigenetics Research Group, Department of Infection and Immunity, Luxembourg Institute of Health (LIH), 29 rue Henri Koch, L-4354 Esch-sur-Alzette, Luxembourg.
Exp Gerontol. 2021 Jul 15;150:111377. doi: 10.1016/j.exger.2021.111377. Epub 2021 Apr 24.
There are many 'faces' of early life adversity (ELA), such as childhood trauma, institutionalisation, abuse or exposure to environmental toxins. These have been implicated in the onset and severity of a wide range of chronic non-communicable diseases later in life. The later-life disease risk has a well-established immunological component. This raises the question as to whether accelerated immune-ageing mechanistically links early-life adversity to the lifelong health trajectory resulting in either 'poor' or 'healthy' ageing. Here we examine observational and mechanistic studies of ELA and inflammageing, highlighting common and distinct features in these two life stages. Many biological processes appear in common including reduction in telomere length, increased immunosenescence, metabolic distortions and chronic (viral) infections. We propose that ELA shapes the developing immune, endocrine and nervous system in a non-reversible way, creating a distinct phenotype with accelerated immunosenescence and systemic inflammation. We conclude that ELA might act as an accelerator for inflammageing and age-related diseases. Furthermore, we now have the tools and cohorts to be able to dissect the interaction between ELA and later life phenotype. This should, in the near future, allow us to identify the ecological and mechanistic processes that are involved in 'healthy' or accelerated immune-ageing.
早期生活逆境（ELA）有许多“面孔”，例如儿童期创伤、机构化、虐待或接触环境毒素。这些都与一生中广泛的慢性非传染性疾病的发病和严重程度有关。晚年疾病风险有一个既定的免疫学成分。这就提出了一个问题，即加速的免疫衰老是否从机制上将早期生活逆境与导致“较差”或“健康”衰老的终身健康轨迹联系起来。在这里，我们研究了 ELA 和炎症衰老的观察性和机制性研究，突出了这两个生命阶段的共同和独特特征。许多生物过程似乎是共同的，包括端粒长度缩短、免疫衰老增加、代谢扭曲和慢性（病毒）感染。我们提出，ELA 以不可逆转的方式塑造正在发育的免疫、内分泌和神经系统，形成具有加速免疫衰老和全身炎症的独特表型。我们得出的结论是，ELA 可能是炎症衰老和与年龄相关疾病的加速因素。此外，我们现在有工具和队列来能够剖析 ELA 和晚年表型之间的相互作用。这应该在不久的将来，使我们能够确定涉及“健康”或加速免疫衰老的生态和机制过程。
