Author: Wong JY1, De Vivo I2, Lin X3, Fang SC4, Christiani DC5.
Affiliation:
1Harvard School of Public Health, Department of Epidemiology, Boston, Massachusetts, United States of America ; Harvard School of Public Health, Department of Environmental Health, Boston, Massachusetts, United States of America ; Brigham and Women's Hospital, Channing Division of Network Medicine, Boston, Massachusetts, United States of America. 2Harvard School of Public Health, Department of Epidemiology, Boston, Massachusetts, United States of America ; Brigham and Women's Hospital, Channing Division of Network Medicine, Boston, Massachusetts, United States of America ; Harvard Medical School, Department of Medicine, Boston, Massachusetts, United States of America. 3Harvard School of Public Health, Department of Biostatistics, Boston, Massachusetts, United States of America. 4Harvard School of Public Health, Department of Environmental Health, Boston, Massachusetts, United States of America ; New England Research Institutes, Watertown, Massachusetts, United States of America. 5Harvard School of Public Health, Department of Environmental Health, Boston, Massachusetts, United States of America ; Massachusetts General Hospital, Boston, Massachusetts, United States of America ; Harvard Medical School, Department of Medicine, Boston, Massachusetts, United States of America.
Conference/Journal: PLoS One.
Date published: 2014 Jan 27
Other:
Volume ID: 9 , Issue ID: 1 , Pages: e87348 , Special Notes: doi: 10.1371/journal.pone.0087348 , Word Count: 276
Abstract
BACKGROUND:
Chronic inflammation from recurring trauma is an underlying pathophysiological basis of numerous diseases. Furthermore, it may result in cell death, scarring, fibrosis, and loss of tissue function. In states of inflammation, subsequent increases in oxidative stress and cellular division may lead to the accelerated erosion of telomeres, crucial genomic structures which protect chromosomes from decay. However, the association between plasma inflammatory marker concentrations and telomere length has been inconsistent in previous studies.
OBJECTIVE:
THE PURPOSE OF THIS STUDY WAS TO DETERMINE THE LONGITUDINAL ASSOCIATION BETWEEN TELOMERE LENGTH AND PLASMA INFLAMMATORY BIOMARKER CONCENTRATIONS INCLUDING: CRP, SAA, sICAM-1, sVCAM-1, VEGF, TNF-α, IL-1β, IL-2, IL-6, IL-8, and IL-10.
METHODS:
The longitudinal study population consisted of 87 subjects. The follow-up period was approximately 2 years. Plasma inflammatory biomarker concentrations were assessed using highly sensitive electrochemiluminescent assays. Leukocyte relative telomere length was assessed using Real-Time qPCR. Linear mixed effects regression models were used to analyze the association between repeated-measurements of relative telomere length as the outcome and each inflammatory biomarker concentration as continuous exposures separately. The analyses controlled for major potential confounders and white blood cell differentials.
RESULTS:
At any follow-up time, each incremental ng/mL increase in plasma CRP concentration was associated with a decrease in telomere length of -2.6×10(-2) (95%CI: -4.3×10(-2), -8.2×10(-3), p = 0.004) units. Similarly, the estimate for the negative linear association between SAA and telomere length was -2.6×10(-2) (95%CI:-4.5×10(-2), -6.1×10(-3), p = 0.011). No statistically significant associations were observed between telomere length and plasma concentrations of pro-inflammatory interleukins, TNF-α, and VEGF.
CONCLUSIONS:
Findings from this study suggest that increased systemic inflammation, consistent with vascular injury, is associated with decreased leukocyte telomere length.
PMID: 24475279
