Effects of maternal type 1 diabetes and confounding factors on neonatal microbiomes
Authors' conclusion
These findings indicate that, in addition to maternal type 1 diabetes, glycaemic dysregulation before/in the first trimester of pregnancy, mode of delivery and intrapartum antibiotic prophylaxis may contribute to the inoculation and formation of the neonatal microbiomes.
Study context
- Population
- Maternal-neonatal dyads; vaginal, rectal and ear-skin swabs and stool samples with clinical metadata from pregnancy and delivery
- Participants
- 92 maternal-neonatal dyads
- Comparison
- Maternal T1D vs control mothers and their neonates
- T1Dn = 50
- Outcome
- Neonatal microbiome composition and determinants
Methodological details16S rRNA amplicon sequencing
- 16S rRNA amplicon sequencing
Main finding
As reported in the abstract
- Influence of delivery mode and intrapartum antibiotic prophylaxis on neonatal microbiota composition
- both p=0.001
- Neonatal ear-skin microbiome variation explained by maternal T1D status (logistic regression, all confounders)
- p=0.020
- Neonatal ear-skin microbiome variation explained by small for gestational age birthweight
- p=0.050
- In T1D, first-trimester HbA1c >55 mmol/mol (>7.2%) related to neonatal ear-skin microbiota composition
- p=0.008
Observational data: associations, not effects.
Further findings
Contribution of maternal rectum microbiota to ear-skin samples of vaginally delivered neonates
Contribution of maternal cervix microbiota to ear-skin samples of vaginally delivered neonates
- Contribution of maternal rectum microbiota to ear-skin samples of vaginally delivered neonates: increase with T1D
- Contribution of maternal cervix microbiota to ear-skin samples of vaginally delivered neonates: decrease with T1D
Predicted microbial functional profiles (PICRUSt)
- Carbohydrate biosynthesis pathways predicted as key dysregulated elements in T1D
Neonatal microbiota attributed to maternal sources (SourceTracker)
- Average share of neonatal microbiota from maternal sources
- 81.0%
Original publication
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