Department of Epidemiology, The Gillings School of Global Public Health, University of North Carolina at Chapel Hill.
Department of Sociology and Carolina Population Center, University of North Carolina at Chapel Hill.
J Gerontol A Biol Sci Med Sci. 2020 Jun 18;75(7):1258-1266. doi: 10.1093/gerona/glaa122.
Emerging links between gut microbiota and diseases of aging point to possible shared immune, metabolic, and cellular damage mechanisms, operating long before diseases manifest. We conducted 16S rRNA sequencing of fecal samples collected from a subsample (n = 668) of Add Health Wave V, a nationally representative longitudinal study of adults aged 32-42. An overlapping subsample (n = 345) included whole-blood RNA-seq. We examined associations between fecal taxonomic abundances and dried blood spot-based markers of lipid and glucose homeostasis and C-reactive protein (measured in Wave IV), as well as gene expression markers of inflammation, cellular damage, immune cell composition, and transcriptomic age (measured in Wave V), using Bayesian hierarchical models adjusted for potential confounders. We additionally estimated a co-abundance network between inflammation-related genes and bacterial taxa using penalized Gaussian graphical models. Strong and consistent microbiota associations emerged for HbA1c, glucose, C-reactive protein, and principal components of genes upregulated in inflammation, DNA repair, and reactive oxygen species, with Streptococcus infantis, Pseudomonas spp., and Peptoniphilus as major players for each. This pattern was largely echoed (though attenuated) for immunological cell composition gene sets, and only Serratia varied meaningfully by transcriptomic age. Network co-abundance indicated relationships between Prevotella sp., Bacteroides sp., and Ruminococcus sp. and gut immune/metabolic regulatory activity, and Ruminococcus sp, Dialister, and Butyrivibrio crossotus with balance between Th1 and Th2 inflammation. In conclusion, many common associations between microbiota and major physiologic aging mechanisms are evident in early-mid adulthood and suggest avenues for early detection and prevention of accelerated aging.
肠道微生物群与衰老相关疾病之间的新联系表明,可能存在共同的免疫、代谢和细胞损伤机制,这些机制早在疾病表现之前就已经存在。我们对来自 Add Health Wave V 的粪便样本的亚样本(n=668)进行了 16S rRNA 测序,这是一项针对 32-42 岁成年人的全国性纵向研究。一个重叠的亚样本(n=345)包括全血 RNA-seq。我们使用贝叶斯层次模型,通过调整潜在的混杂因素,检验了粪便分类丰度与基于干血斑的脂质和葡萄糖稳态标志物以及 C 反应蛋白(在第四波测量)之间的关联,以及炎症、细胞损伤、免疫细胞组成和转录组年龄的基因表达标志物(在第五波测量)。我们还使用惩罚高斯图形模型估计了与炎症相关基因和细菌分类群之间的共同丰度网络。HbA1c、葡萄糖、C 反应蛋白和炎症、DNA 修复和活性氧上调基因的主要成分的基因表达水平与肠道微生物群之间存在强烈且一致的关联,其中婴儿链球菌、假单胞菌和消化链球菌是每个基因的主要参与者。这种模式在很大程度上(尽管有所减弱)与免疫细胞组成基因集相呼应,只有血清变形菌的转录组年龄有显著差异。网络共同丰度表明,普雷沃氏菌属、拟杆菌属和真杆菌属之间存在关系,以及肠道免疫/代谢调节活性,以及真杆菌属、Dialister 和 Butyrivibrio crossotus 与 Th1 和 Th2 炎症之间的平衡。总之,在成年早期和中期,肠道微生物群与主要生理衰老机制之间存在许多共同关联,这为早期检测和预防加速衰老提供了途径。