Abstract
Cross talk between the intestinal microbiome and the lung and its role in lung health remains unknown. Perinatal exposure to antibiotics disrupts the neonatal microbiome and may have an impact on the preterm lung. We hypothesized that perinatal antibiotic exposure leads to long-term intestinal dysbiosis and increased alveolar simplification in a murine hyperoxia model. Pregnant C57BL/6 wild type dams and neonatal mice were treated with antibiotics before and/or immediately after delivery. Control mice received phosphate-buffered saline (PBS). Neonatal mice were exposed to 95% oxygen for 4 days or room air. Microbiome analysis was performed using 16S rRNA gene sequencing. Pulmonary alveolarization and vascularization were analyzed at postnatal day (PND) 21. Perinatal antibiotic exposure modified intestinal beta diversity but not alpha diversity in neonatal mice. Neonatal hyperoxia exposure altered intestinal beta diversity and relative abundance of commensal bacteria in antibiotic treated mice. Hyperoxia disrupted pulmonary alveolarization and vascularization at PND 21; however, there were no differences in the degree of lung injury in antibiotic treated mice compared to vehicle treated controls. Our study suggests that exposure to both hyperoxia and antibiotics early in life may cause long-term alterations in the intestinal microbiome, but intestinal dysbiosis may not significantly influence neonatal hyperoxic lung injury.
Highlights
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that remains one of the most common long-term complications of preterm birth
There has been an increase in survival of extremely premature infants over time, the incidence of BPD remains stagnant despite advances in care[1]
Our study found that antibiotics cause long term changes in the composition of the intestinal microbiome
Summary
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that remains one of the most common long-term complications of preterm birth. It results from a complex, multifactorial process that disrupts alveolar growth and pulmonary vascular development in the preterm infant lung[1]. Factors influencing this disruption include prematurity, hyperoxia, inflammation, prenatal and postnatal infections, mechanical ventilation, and growth restriction, amongst others. The preterm microbiome potentially impacts neonatal disease and long-term health outcomes of premature infants. We hypothesize that perinatal antibiotic-mediated intestinal dysbiosis increases BPD-like phenotype in a murine hyperoxia model
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
