Background Prematurity in itself and exposure to neonatal intensive care triggers inflammatory processes and oxidative stress, leading to risk for disease later in life. The effects on cellular aging processes are incompletely understood. Methods Relative telomere length (RTL) was measured by qPCR in this longitudinal cohort study with blood samples taken at birth and at 2 years of age from 60 children (16 preterm and 44 term). Viral respiratory infections the first year were evaluated. Epigenetic biological DNA methylation (DNAm) age was predicted based on methylation array data in 23 children (11 preterm and 12 term). RTL change/year and DNAm age change/year was compared in preterm and term during the 2 first years of life. Results Preterm infants had longer telomeres than term born at birth and at 2 years of age, but no difference in telomere attrition rate could be detected. Predicted epigenetic DNAm age was younger in preterm infants, but rate of DNAm aging was similar in both groups. Conclusions Despite early exposure to risk factors for accelerated cellular aging, children born preterm exhibited preserved telomeres. Stress during the neonatal intensive care period did not reflect accelerated epigenetic DNAm aging. Early-life aging was not explained by preterm birth. Impact Preterm birth is associated with elevated disease risk later in life. Preterm children often suffer from inflammation early in life. Stress-related telomere erosion during neonatal intensive care has been proposed. Inflammation-accelerated biological aging in preterm is unknown. We find no accelerated aging due to prematurity or infections during the first 2 years of life.

中文翻译：

---

早产儿在出生后的头 2 年内不会加速造血细胞衰老

背景 早产本身和新生儿重症监护会引发炎症过程和氧化应激，从而导致生命后期患病的风险。对细胞衰老过程的影响尚不完全清楚。方法 在这项纵向队列研究中，通过 qPCR 测量相对端粒长度 (RTL)，血液样本在出生时和 2 岁时从 60 名儿童（16 名早产儿和 44 名足月儿）中采集。评估第一年的病毒性呼吸道感染。根据 23 名儿童（11 名早产儿和 12 名足月儿）的甲基化阵列数据预测表观遗传生物 DNA 甲基化 (DNAm) 年龄。在生命的最初 2 年，比较早产和足月的 RTL 变化/年和 DNAm 年龄变化/年。结果 早产儿的端粒比出生时和 2 岁时的足月儿长，但没有检测到端粒磨损率的差异。早产儿预测的表观遗传 DNAm 年龄较小，但两组的 DNAm 衰老率相似。结论 尽管早期暴露于加速细胞衰老的风险因素，早产儿仍表现出保留的端粒。新生儿重症监护期间的压力并未反映表观遗传 DNAm 加速老化。早产不能解释生命早期衰老。影响 早产与晚年疾病风险升高有关。早产儿通常在生命早期就患有炎症。已经提出了新生儿重症监护期间与压力相关的端粒侵蚀。早产儿炎症加速的生物老化是未知的。我们发现在生命的前 2 年中没有由于早产或感染而加速衰老。