Abstract
Leukocyte telomere length is a biomarker of aging-related health risks. Hospitalized preterm infants frequently experience elevated oxidative stress and inflammation, both of which contribute to telomere shortening. Our aim was to examine changes in telomere length during neonatal intensive care unit (NICU) hospitalization in a cohort of preterm infants <32 weeks’ gestation. We conducted a longitudinal study of 10 infants (mean gestational age 27 weeks, range 23.5 to 29, at birth). We isolated DNA from dried blood spots and used Real Time Quantitative PCR to measure relative leukocyte telomere length in triplicate at three time points for each participant. From birth to discharge, infants experienced an average decline in relative telomere length of 0.021 units per week (95% CI -0.040, -0.0020; p = 0.03), after adjustment for gestational age at birth. Our results suggest a measurable decline in telomere length during NICU hospitalization. We speculate that telomere length change may convey information about NICU exposures that carry short- and long-term health risks.
Highlights
Telomeres are repeating nucleotide sequences of variable number that protect against chromosome deterioration and regulate cellular and tissue function [1]
Most prior telomere research has focused on adult populations, telomere attrition may be prominent in early life, as shown in studies of childhood adversities [11]
We detected little difference in relative telomere length according to gestational age at birth (0.004 units per week, 95% CI -0.040, 0.049, p = 0.8)
Summary
Telomeres are repeating nucleotide sequences of variable number that protect against chromosome deterioration and regulate cellular and tissue function [1]. Telomere attrition is a wellestablished biomarker of aging. Shorter telomere length is associated with earlier mortality [2], impaired cognitive function [3], cardiovascular disease [4,5], and chronic obstructive pulmonary disease [6]. While heritable to some extent [7], the rate of telomere attrition is susceptible to environmental influences, with effects mediated, at least in part, by oxidative stress [8] and inflammation [9,10].
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