Abstract
BackgroundIn this study, we aimed to analyze differences in plasma protein abundances between infants with and without bronchopulmonary dysplasia (BPD), to add new insights into a better understanding of the pathogenesis of this disease.MethodsCord and peripheral blood of neonates (≤ 30 weeks gestational age) was drawn at birth and at the 36th postmenstrual week (36 PMA), respectively. Blood samples were retrospectively subdivided into BPD(+) and BPD(−) groups, according to the development of BPD.ResultsChildren with BPD were characterized by decreased afamin, gelsolin and carboxypeptidase N subunit 2 levels in cord blood, and decreased galectin-3 binding protein and hemoglobin subunit gamma-1 levels, as well as an increased serotransferrin abundance in plasma at the 36 PMA.ConclusionsBPD development is associated with the plasma proteome changes in preterm infants, adding further evidence for the possible involvement of disturbances in vitamin E availability and impaired immunological processes in the progression of prematurity pulmonary complications. Moreover, it also points to the differences in proteins related to infection resistance and maintaining an adequate level of hematocrit in infants diagnosed with BPD.
Highlights
In this study, we aimed to analyze differences in plasma protein abundances between infants with and without bronchopulmonary dysplasia (BPD), to add new insights into a better understanding of the pathogenesis of this disease
We described the comparison between abundances of all plasma proteins from prematurely born children with different gestational ages, both from cord blood as well as at the 36th postmenstrual week (36 Postmenstrual week (PMA)) [7,8,9]
We published data describing the differences in plasma protein abundances in prematurely born infants with and without retinopathy of prematurity (ROP) [10]
Summary
We aimed to analyze differences in plasma protein abundances between infants with and without bronchopulmonary dysplasia (BPD), to add new insights into a better understanding of the pathogenesis of this disease. Despite indubitable improvements in neonatal care, bronchopulmonary dysplasia (BPD) remains a most frequent, adverse outcome of prematurity [1]. We described the comparison between abundances of all plasma proteins from prematurely born children with different gestational ages, both from cord blood as well as at the 36th postmenstrual week (36 PMA) [7,8,9]. We published data describing the differences in plasma protein abundances in prematurely born infants with and without retinopathy of prematurity (ROP) [10]
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