背景:低等级,衰老过程中的慢性炎症,(“发炎”),建议参与老年衰弱的发展。然而,关于脆弱之间关联的研究,使用脆弱索引定义,和炎症标志物是有限的。这项研究的目的是调查炎症标志物和衰弱指数(FI)之间的关系,家庭居住的成年人。
方法:家庭男女年龄≥70岁,我们招募了居住在挪威东南部的人,并纳入了一项横断面研究.当前研究中使用的FI是根据Rockwood的脆弱指数开发的,包括38个变量,导致每个参与者的FI得分在0到1之间。循环炎症标志物(IL-6,CRP,IGF-1,胱抑素C,组织蛋白酶S,和糖蛋白乙酰)使用ELISA分析非空腹血液样品。使用全基因组PBMC转录组学研究FI评分与炎症之间的关联。
结果:研究人群包括403名老年人(52%为女性),年龄中位数为74岁,平均BMI为26.2kg/m2。全组的平均FI评分为0.15(范围0.005-0.56)。将其分为虚弱组(FI评分≥0.25)和非虚弱组。调整BMI后,年龄,性别,在整个小组中吸烟,IL-6,组织蛋白酶S,胱抑素C,和Gp-乙酰基仍然与FI评分显着相关(IL-6:0.002,95%CI:0.001,0.002,组织蛋白酶S:6.7e-06,95%CI2.44e-06,0.00001,胱抑素C:0.004,95%CI:0.002,0.006,Gp-乙酰基:0.09,95%CI:0.05,0.13,所有p<0.01),而CRP和IGF-1则没有(0.0003,95%CI:-00001,0.0007,p=0.13,(-1.27e-06),95%CI:(-0.0003),0.0003,p=0.99)。FI评分和炎症标志物之间存在显著关联,和FI评分和单核细胞特异性基因表达。
结论:我们发现FI评分与炎症标志物之间存在关联,以及70岁以上老年受试者的FI评分和单核细胞特异性基因表达之间的差异。炎症是否是虚弱的原因或结果,以及虚弱的进展是否可以通过减少炎症而减弱,还有待澄清。
BACKGROUND: Low-grade, chronic inflammation during ageing, (\"inflammageing\"), is suggested to be involved in the development of frailty in older age. However, studies on the association between frailty, using the frailty index definition, and inflammatory markers are limited. The aim of this study was to investigate the relationship between inflammatory markers and frailty index (FI) in older, home-dwelling adults.
METHODS: Home-dwelling men and women aged ≥ 70 years old, living in South-East Norway were recruited and included in a cross-sectional study. The FI used in the current study was developed according to Rockwood\'s frailty index and included 38 variables, resulting in an FI score between 0 and 1 for each participant. Circulating inflammatory markers (IL-6, CRP, IGF-1, cystatin C, cathepsin S, and glycoprotein Acetyls) were analyzed from non-fasting blood samples using ELISA. Whole-genome PBMC transcriptomics was used to study the association between FI score and inflammation.
RESULTS: The study population comprised 403 elderly (52% women), with a median age of 74 years and a mean BMI of 26.2 kg/m2. The mean FI score for the total group was 0.15 (range 0.005-0.56). The group was divided into a frail group (FI score ≥ 0.25) and non-frail group. After adjusting for BMI, age, sex, and smoking in the whole group, IL-6, cathepsin S, cystatin C, and Gp-acetyls remained significant associated to FI score (IL-6: 0.002, 95% CI: 0.001, 0.002, cathepsin S: 6.7e-06, 95% CI 2.44e-06, 0.00001, cystatin C: 0.004, 95% CI: 0.002, 0.006, Gp- Acetyls: 0.09, 95% CI: 0.05, 0.13, p < 0.01 for all), while CRP and IGF-1 were not (0.0003, 95% CI: -00001, 0.0007, p = 0.13, (-1.27e-06), 95% CI: (-0.0003), 0.0003, p = 0.99). There was a significant association between FI score and inflammatory markers, and FI score and monocyte-specific gene expression.
CONCLUSIONS: We found an association between FI score and inflammatory markers, and between FI score and monocyte-specific gene expression among elderly subjects above 70 years of age. Whether inflammation is a cause or consequence of frailty and whether the progression of frailty can be attenuated by reducing inflammation remains to be clarified.