Hematopoietic cellular aging is not accelerated during the first 2 years of life in children born preterm

Area of Science:

• Pediatrics
• Genetics
• Developmental Biology

Background:

• Prematurity and neonatal intensive care are linked to inflammation and oxidative stress, potentially increasing later-life disease risk.
• The impact of these factors on cellular aging processes in early life remains incompletely understood.
• Understanding biological aging in preterm infants is crucial for addressing long-term health disparities.

Purpose of the Study:

• To investigate the effects of prematurity on cellular aging markers, specifically relative telomere length (RTL) and epigenetic DNA methylation (DNAm) age, during the first two years of life.
• To compare the rate of telomere attrition and DNAm aging between preterm and term-born infants.
• To determine if early-life stress associated with prematurity accelerates biological aging.

Main Methods:

• A longitudinal cohort study measured RTL using qPCR in blood samples from 60 children (16 preterm, 44 term) at birth and 2 years.
• Viral respiratory infections in the first year were recorded.
• Epigenetic DNAm age was predicted using methylation array data in a subset of 23 children (11 preterm, 12 term).

Main Results:

• Preterm infants exhibited longer telomeres at both birth and 2 years compared to term infants.
• No significant difference in the rate of telomere attrition was detected between the groups.
• Preterm infants had a younger predicted epigenetic DNAm age, but their rate of DNAm aging was similar to term infants.

Conclusions:

• Children born preterm demonstrated preserved telomeres and no accelerated epigenetic aging in the first two years, despite early-life risk factors.
• Neonatal intensive care stress did not correlate with accelerated epigenetic DNAm aging in this cohort.
• Preterm birth and early infections did not appear to explain accelerated early-life biological aging within the observed timeframe.