ArticleERJ open research2026
Airway microbial dysbiosis and oxidative mitochondrial DNA damage in the development of bronchopulmonary dysplasia.
Article in ERJ open research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
10 authors.
Funding
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Abstract
Background: This study investigated the association between airway microbiome composition, oxidative mitochondrial DNA (mtDNA) damage and the development of bronchopulmonary dysplasia (BPD) in preterm infants. Methods: A prospective cohort study enrolled 82 very low birth weight preterm infants (<32 weeks' gestation). Tracheal aspirates (TA) were collected at birth and on postnatal day 28. Airway microbial diversity and composition were assessed using 16S rRNA sequencing. Oxidative mtDNA damage was measured using 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in TA samples. We used PICRUSt2-based metagenome predictions from 16S rRNA gene sequencing of TA samples, with functional pathway annotations based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Results: Infants who developed BPD (n=25) had lower gestational age, birth weight and prolonged ventilatory support (p<0.05). Oxidative mtDNA damage was significantly higher in infants with BPD, particularly in moderate-to-severe cases (p<0.05). BPD was associated with reduced microbial alpha diversity and distinct beta diversity clustering. Infants with BPD exhibited higher relative abundance of Proteobacteria and lower relative abundance of Conclusions: Airway microbial dysbiosis and oxidative mtDNA damage are strongly associated with BPD severity. Targeting oxidative stress and microbiome modulation may offer potential strategies for BPD prevention and management.
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Registered trials
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