Bauer Moisés E, Jeckel Cristina M Moriguchi, Luz Clarice
Faculdade de Biociências and Instituto de Pesquisas Biomédicas, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil.
Ann N Y Acad Sci. 2009 Feb;1153:139-52. doi: 10.1111/j.1749-6632.2008.03966.x.
This manuscript reviews current evidence suggesting that aging of the immune system (immunosenescence) may be closely related to chronic stress and stress factors. Healthy aging has been associated with emotional distress in parallel to increased cortisol to dehydroepiandrosterone (DHEA) ratio. The impaired DHEA secretion together with the increase of cortisol results in an enhanced exposure of lymphoid cells to deleterious glucocorticoid actions. The lack of appropriated growth hormone signaling during immunosenescence is also discussed. It follows that altered neuroendocrine functions could be underlying several immunosenescence features. Indeed, changes in both innate and adaptive immune responses during aging are also similarly reported during chronic glucocorticoid exposure. In addition, chronically stressed elderly subjects may be particularly at risk of stress-related pathology because of further alterations in both neuroendocrine and immune systems. The accelerated senescent features induced by chronic stress include higher oxidative stress, reduced telomere length, chronic glucocorticoid exposure, thymic involution, changes in cellular trafficking, reduced cell-mediated immunity, steroid resistance, and chronic low-grade inflammation. These senescent features are related to increased morbidity and mortality among chronically stressed elderly people. Overall, these data suggest that chronic stress leads to premature aging of key allostatic systems involved in the adaptation of the organisms to environmental changes. Stress management and psychosocial support may thus promote a better quality of life for elderly people and at the same time reduce hospitalization costs.
本手稿回顾了当前的证据，表明免疫系统衰老（免疫衰老）可能与慢性应激和应激因素密切相关。健康衰老与情绪困扰相关，同时皮质醇与脱氢表雄酮（DHEA）的比值增加。DHEA分泌受损以及皮质醇增加导致淋巴细胞更多地暴露于有害的糖皮质激素作用之下。文中还讨论了免疫衰老过程中生长激素信号传导缺失的情况。由此可见，神经内分泌功能改变可能是多种免疫衰老特征的潜在原因。事实上，衰老过程中固有免疫和适应性免疫反应的变化在慢性糖皮质激素暴露期间也有类似报道。此外，由于神经内分泌和免疫系统的进一步改变，长期处于应激状态的老年受试者可能特别容易出现与应激相关的病理状况。慢性应激诱导的加速衰老特征包括更高的氧化应激、端粒长度缩短、慢性糖皮质激素暴露、胸腺退化、细胞转运变化、细胞介导免疫降低、类固醇抵抗和慢性低度炎症。这些衰老特征与长期处于应激状态的老年人发病率和死亡率增加有关。总体而言，这些数据表明慢性应激会导致参与生物体适应环境变化的关键稳态系统过早衰老。因此，压力管理和社会心理支持可能会提高老年人的生活质量，同时降低住院费用。
