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Published on: August 7, 2017
Microbial signatures in amniotic fluid at preterm birth and association with bronchopulmonary dysplasia
Birte Staude1,2, Silvia Gschwendtner3, Tina Frodermann1
1Department of General Pediatrics and Neonatology, Justus Liebig University and Universities of Giessen and Marburg Lung Center, Giessen, Germany.
Insights
Prenatal amniotic fluid bacterial signatures differ in preterm infants, potentially identifying those at risk for bronchopulmonary dysplasia (BPD). These distinct microbial patterns highlight the prenatal origins of BPD.
Area of Science:
- Microbiology
- Neonatalogy
- Genetics
Background:
- Microbiome dysbiosis is linked to various diseases, including bronchopulmonary dysplasia (BPD).
- Intra-amniotic infection is a key risk factor for BPD, a multifactorial disease.
- Recent studies associate lung microbiota colonization with BPD development.
Purpose of the Study:
- To compare bacterial signatures in amniotic fluid (AF) from intact pregnancies versus preterm deliveries.
- To analyze variations in AF bacterial signatures across different BPD severity stages.
Main Methods:
- Prospective observational cohort study.
- Collected AF samples from intact pregnancies (n=17) and preterm deliveries (<32 weeks, n=126).
- Utilized 16S rRNA gene metabarcoding to assess bacterial community structure.
Main Results:
- Preterm delivery AF showed increased 16S rRNA genes, reduced alpha diversity, and altered beta diversity.
- Lactobacillus and Acetobacter were less abundant, while Fusobacterium, Pseudomonas, Ureaplasma, and Staphylococcus were more prevalent.
- Moderate/severe BPD AF had Escherichia-Shigella, mild BPD AF had Ureaplasma and Enterococcus enrichment.
Conclusions:
- Distinct intrauterine bacterial 16S rRNA gene patterns were identified in preterm infants.
- These prenatal microbial signatures differ from those in intact pregnancies.
- The findings emphasize the prenatal impact on BPD origins and identify potential risk indicators.
Background:
Microbiome dysbiosis can have long-lasting effects on our health and induce the development of various diseases. Bronchopulmonary dysplasia (BPD) is a multifactorial disease with pre- and postnatal origins including intra-amniotic infection as main risk factor. Recently, postnatal pathologic lung microbiota colonization was associated with BPD. The objectives of this prospective observational cohort study were to describe differences in bacterial signatures in the amniotic fluid (AF) of intact pregnancies without clinical signs or risk of preterm delivery and AF samples obtained during preterm deliveries and their variations between different BPD disease severity stages.
Methods:
AF samples were collected under sterile conditions during fetal intervention from intact pregnancies (n = 17) or immediately before preterm delivery < 32 weeks (n = 126). Metabarcoding based approaches were used for the molecular assessment of bacterial 16S rRNA genes to describe bacterial community structure.
Results:
The absolute amount of 16S rRNA genes was significantly increased in AF of preterm deliveries and detailed profiling revealed a reduced alpha diversity and a significant change in beta diversity with a reduced relative abundance of 16S rRNA genes indicative for Lactobacillus and Acetobacter while Fusobacterium, Pseudomonas, Ureaplasma and Staphylococcus 16S rRNA gene prevailed. Although classification of BPD by disease severity revealed equivalent absolute 16S rRNA gene abundance and alpha and beta diversity in no, mild and moderate/severe BPD groups, for some 16S rRNA genes differences were observed in AF samples. Bacterial signatures of infants with moderate/severe BPD showed predominance of 16S rRNA genes belonging to the Escherichia-Shigella cluster while Ureaplasma and Enterococcus species were enriched in AF samples of infants with mild BPD.
Conclusions:
Our study identified distinct and diverse intrauterine 16S rRNA gene patterns in preterm infants immediately before birth, differing from the 16S rRNA gene signature of intact pregnancies. The distinct 16S rRNA gene signatures at birth derive from bacteria with varying pathogenicity to the immature lung and are suited to identify preterm infants at risk. Our results emphasize the prenatal impact to the origins of BPD.
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