Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil; Departamento de Medicina, Universidade Federal de Juiz de Fora, Governador Valadares, Brazil.
Mech Ageing Dev. 2022 Oct;207:111713. doi: 10.1016/j.mad.2022.111713. Epub 2022 Aug 2.
Inflammaging is a low-grade inflammatory state generated by the aging process that can contribute to frailty and age-related diseases in the elderly. However, it can have distinct effects in the elderly living in endemic areas for infectious diseases. An increased inflammatory response may confer protection against infectious agents in these areas, although this advantage can cause accelerating epigenetic aging. In this study, we evaluated the inflammatory profile and the epigenetic age of infected and noninfected individuals from an endemic area in Brazil. The profile of cytokines, chemokines and growth factors analyzed in the sera of the two groups of individuals showed similarities, although infected individuals had a higher concentration of these mediators. A significant increase in IL-1ra, CXCL8, CCL2, CCL3 and CCL4 production was associated with leprosy infection. Notably, elderly individuals displayed distinct immune responses associated with their infection status when compared to adults suggesting an adaptive remodelling of their immune responses. Epigenetic analysis also showed that there was no difference in epigenetic age between the two groups of individuals. However, individuals from the endemic area had a significant accelerated aging when compared to individuals from São Paulo, a non-endemic area in Brazil. Moreover, the latter cohort was also epigenetically aged in relation to an Italian cohort. Our data shows that living in endemic areas for chronic infectious diseases results in remodelling of inflammaging and acceleration of epigenetic aging in individuals regardless of their infectious status. It also highlights that geographical, genetic and environmental factors influence aging and immunosenescence in their pace and profile.
炎症衰老(Inflammaging)是由衰老过程产生的低度炎症状态,可导致老年人脆弱和与年龄相关的疾病。然而,在传染病流行地区生活的老年人中,它可能会产生截然不同的影响。在这些地区,增加的炎症反应可能对感染因子提供保护,尽管这种优势可能导致表观遗传加速衰老。在这项研究中,我们评估了巴西一个传染病流行地区感染和未感染个体的炎症特征和表观年龄。对两组个体血清中分析的细胞因子、趋化因子和生长因子的特征表明,两组之间存在相似性,尽管感染个体的这些介质浓度更高。IL-1ra、CXCL8、CCL2、CCL3 和 CCL4 的产生显著增加与麻风病感染有关。值得注意的是,与成年人相比,老年个体表现出与感染状态相关的不同免疫反应,表明其免疫反应发生了适应性重塑。表观遗传分析还表明,两组个体之间的表观年龄没有差异。然而,与来自巴西非传染病流行地区圣保罗的个体相比,来自流行地区的个体的表观年龄显著加速。此外,与意大利队列相比,后者队列的表观年龄也加速了。我们的数据表明,生活在慢性传染病流行地区会导致炎症衰老的重塑,并加速无论其感染状态如何的个体的表观遗传衰老。它还强调了地理、遗传和环境因素会影响衰老和免疫衰老的速度和特征。