Soluble ICAM-1, independent of IL-6, is associated with prevalent frailty in community-dwelling elderly Taiwanese people

Wei Ju Lee, Liang Kung Chen, Chih Kuang Liang, Li Ning Peng, Shu Ti Chiou, Pesus Chou

研究成果: Article同行評審

33 引文 斯高帕斯(Scopus)

摘要

Background: Activation of inflammatory pathway with elevation of inflammatory biomarkers such as Interleukin 6 (IL-6) has been considered a pathophysiological feature of frailty. In recent years, the association between Intercellular adhesive molecule -1 (ICAM-1) and vascular inflammatory was established. Provocation of inflammatory cascades from ICAM-1 is potential IL-6 related, although the association between the inflammatory process and frailty is little to known. The study was intended to evaluate the relationship between serum ICAM-1, IL-6 and frailty. Materials and Methods: Data was derived from a representative national sampling cohort in Taiwan. The cross-sectional study included nine-hundred-forty-six community-dwelling people aged 53 and older. Frailty was defined as having three or more components (including, muscle shrinkage, slowness, weakness, exhaustion, and low activity) Serum IL-6 and ICAM-1 levels were measured using standard enzyme-linked immunosorbent assays. Results: Soluble ICAM-1 (sICAM-1) levels were stepwise increased in non-frail, pre-frail and frail elderly people (the median levels were 255 vs. 265 vs. 285 ng/ml, respectively p<0.001). A multivariate multinomial logistic regression, which was adjusted for age, sex, smoking, education, BMI, and chronic disease number, was utilized to determine that the probability of being frail due to increased log (ICAM-1) and log (IL-6) standard deviation levels were 1.44 (95% CI 1.09-1.91) and 1.54 (95%CI 1.07-2.20), respectively. Conclusion: sICAM-1 was significantly associated with frailty, independent of IL-6. This implied that leukocyte migration and inflammation cascade activation might contribute to frailty, in addition to monocyte/macrophage-mediated immuno-inflammation.

原文English
文章編號e0157877
期刊PLoS ONE
11
發行號6
DOIs
出版狀態Published - 1 6月 2016

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