Abstract
BackgroundModification of the gut microbiota by antibiotics may influence the disease susceptibility and immunological responses. Infants in the neonatal intensive care unit (NICU) subjected to frequent antibiotics and oxygen therapies, which may give rise to local and systemic inflammatory reactions and progression of bronchopulmonary dysplasia (BPD). This study aimed to investigate the role of intestinal dysbacteriosis by antibiotic therapy before hyperoxia exposure in the progression of BPD.MethodsMice had been exposed to hyperoxia (85% O2) since postnatal day 3 until day 16 for the BPD model establishment, treated with antibiotics from postnatal day 2 until day 8. Treated mice and appropriate controls were harvested on postnatal day 2 or 10 for 16S rRNA gene sequencing, or postnatal day 17 for assessment of alveolar morphometry and macrophages differentiation.ResultsAntibiotic-induced intestinal dysbacteriosis before hyperoxia exposure gave rise to deterioration of BPD evidenced by reduced survival rates and alveolarization. Moreover, antibiotic-induced intestinal dysbacteriosis resulted in increased M1 macrophage maker (iNOS) and decreased M2 macrophage maker (Arg-1) levels in lung homogenates.ConclusionBroad-spectrum antibiotic-induced intestinal dysbacteriosis may participate in BPD pathogenesis via alteration of the macrophage polarization status. Manipulating the gut microbiota may potentially intervene the therapy of BPD.
Highlights
As a multi-factorial chronic lung disease of preterm infants, Bronchopulmonary dysplasia (BPD) subjected to interrupted lung deterioration [1]
After seven days of antibiotics therapy, Proteobacteria accounted for a higher proportion at the phylum level, whereas Firmicutes and Bacteroidetes accounted for a reduced proportion in the antibiotics treated mice than that in the saline treated mice (Fig. 2a, b, P < 0.01)
Arg-1 decreased in bronchopulmonary dysplasia (BPD) mice and Antibiotics treatment (ABX) inhibited Arg-1 expression only when mice exposed to hyperoxia (Fig. 4a, P < 0.05)
Summary
As a multi-factorial chronic lung disease of preterm infants, Bronchopulmonary dysplasia (BPD) subjected to interrupted lung deterioration [1]. Infants in the neonatal intensive care unit (NICU) frequently receive antibiotic therapy [3]. Intestinal dysbacteriosis may influence the pulmonary immunological response through the intestinal-pulmonary axis [7, 8]. Modification of the gut microbiota by antibiotics may influence the disease susceptibility and immunological responses. Infants in the neonatal intensive care unit (NICU) subjected to frequent antibiotics and oxygen therapies, which may give rise to local and systemic inflammatory reactions and progression of bronchopulmonary dysplasia (BPD).
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
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 call
