Introduction: Preterm infants are more susceptible to oxidative stress and prone to respiratory diseases in infancy. Cellular autophagy is an important defence mechanism against oxidative stress. It is important for in-utero development and maintenance of a healthy pregnancy and is involved in lung development and respiratory morbidity.

Objectives: We hypothesized that autophagy marker levels differ between preterm and term infants.

Methods: In the prospective Basel-Bern Infant Lung Development (BILD) birth cohort we compared cord blood biomarker levels of macroautophagy (Beclin-1, LC3B), selective autophagy (p62) and regulation of autophagy (SIRT1) in 97 preterm and 561 term infants. We used Tobit regression models adjusted for risk factors (e.g., small for gestational age and mode of delivery) and Spearman?s correlation coefficients.

Results: Beclin-1 and LC3B did not differ between preterm and term infants. However, p62 was higher (0.53, 95% confidence interval (CI) 0.28;0.79 in log2-transformed level, p_adj<0.001) and SIRT1 lower in preterm infants (-0.37, 95% CI -0.56;-0.17 in log2-transformed level, p_adj<0.001). Spearman?s correlation coefficient between p62 and LC3B was stronger in preterm infants (r_s=-0.62, 95% CI -0.73;-0.48, p_adj<0.001) than in term infants (r_s=-0.42, 95% CI -0.49;-0.35, p_adj<0.001).

Conclusion: Our findings suggest differential expression of key autophagy markers between preterm and term infants. This adds to the knowledge of the sparsely studied field of autophagy mechanisms in preterm infants and might be linked to impaired oxidative stress response, preterm birth, impaired lung development and higher susceptibility to respiratory morbidity in preterm infants.