Zhu Mengpei, Huang Yumei, Wang Ziwen, Jin Ze, Cao Jiali, Zhong Qiangqiang, Xiong Zhifan
Institute of Geriatric Medicine, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Division of Gastroenterology, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Aging Dis. 2024 Mar 21;16(2):1180-1198. doi: 10.14336/AD.2024.0321.
Targeting adverse pathogenic gut microbiota regulation through fecal microbiota transplantation (FMT) may restore health and has been validated in some aging-related diseases. However, the mechanisms of the gut microbiota's role in frailty and whether modulation of the gut microbiota can treat age-related frailty remain largely unknown. To assess the effects of FMT on frailty, we used bidirectional fecal microbiota transplantation in young and old mice. We demonstrated that fecal bacteria transplanted from old mice into young mice reduced body weight and grip strength (p=0.002), and led to elevated inflammatory factors in young mice, but had no significant effect on intestinal barrier function. Notably, FMT treatment in older mice not only improved frailty (grip strength: p=0.036, low physical activity: p=0.020, running speed: p=0.048, running time: p=0.058, frailty score: p=0.027) and muscle mass, but also improved intestinal ecological imbalances, intestinal barrier function, and systemic inflammation (serum TNF-α: p=0.002, and IL-6: p<0.001). KEGG enrichment analysis of fecal metabolites showed that FMT may ameliorate frailty through the sphingolipid metabolism pathway. In addition, aged mice given FMT treatment showed a significant increase in the abundance of SCFA-producing bacteria and increased levels of short-chain fatty acids (butyric acid: p=0.084, propionic acid: p=0.028). Subsequent further verification found that FMT ameliorating frailty may be achieved through SCFAs metabolism. Another mechanism study found that FMT reduces lipopolysaccharide levels (p<0.001), thereby inhibiting the TLR4/NF-κB signaling pathway and its downstream pro-inflammatory products. Therefore, regulating SCFAs metabolism by altering gut microbial composition and targeting the gut-muscle axis with LPS/TLR4 pathways may be potential strategies to treat frailty in older adults.
通过粪便微生物群移植(FMT)靶向调节有害致病肠道微生物群可能恢复健康,并且已在一些与衰老相关的疾病中得到验证。然而,肠道微生物群在衰弱中发挥作用的机制以及调节肠道微生物群是否可以治疗与年龄相关的衰弱在很大程度上仍然未知。为了评估FMT对衰弱的影响,我们在年轻和老年小鼠中进行了双向粪便微生物群移植。我们证明,从老年小鼠移植到年轻小鼠体内的粪便细菌降低了体重和握力(p = 0.002),并导致年轻小鼠体内炎症因子升高,但对肠道屏障功能没有显著影响。值得注意的是,对老年小鼠进行FMT治疗不仅改善了衰弱(握力:p = 0.036,低体力活动:p = 0.020,跑步速度:p = 0.048,跑步时间:p = 0.058,衰弱评分:p = 0.027)和肌肉质量,还改善了肠道生态失衡、肠道屏障功能和全身炎症(血清TNF-α:p = 0.002,IL-6:p < 0.001)。粪便代谢物的KEGG富集分析表明,FMT可能通过鞘脂代谢途径改善衰弱。此外,接受FMT治疗的老年小鼠中产生短链脂肪酸的细菌丰度显著增加,短链脂肪酸水平升高(丁酸:p = 0.084,丙酸:p = 0.028)。随后的进一步验证发现,FMT改善衰弱可能是通过短链脂肪酸代谢实现的。另一项机制研究发现,FMT降低了脂多糖水平(p < 0.001),从而抑制了TLR4/NF-κB信号通路及其下游促炎产物。因此,通过改变肠道微生物组成来调节短链脂肪酸代谢以及通过LPS/TLR4途径靶向肠道-肌肉轴可能是治疗老年人衰弱的潜在策略。