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Publication Detail

Title: Perinatal maternal antibiotic exposure augments lung injury in offspring in experimental bronchopulmonary dysplasia.

Authors: Willis, Kent A; Siefker, David T; Aziz, Michael M; White, Catrina T; Mussarat, Naiha; Gomes, Charles K; Bajwa, Amandeep; Pierre, Joseph F; Cormier, Stephania A; Talati, Ajay J

Published In Am J Physiol Lung Cell Mol Physiol, (2020 02 01)

Abstract: During the newborn period, intestinal commensal bacteria influence pulmonary mucosal immunology via the gut-lung axis. Epidemiological studies have linked perinatal antibiotic exposure in human newborns to an increased risk for bronchopulmonary dysplasia, but whether this effect is mediated by the gut-lung axis is unknown. To explore antibiotic disruption of the newborn gut-lung axis, we studied how perinatal maternal antibiotic exposure influenced lung injury in a hyperoxia-based mouse model of bronchopulmonary dysplasia. We report that disruption of intestinal commensal colonization during the perinatal period promotes a more severe bronchopulmonary dysplasia phenotype characterized by increased mortality and pulmonary fibrosis. Mechanistically, metagenomic shifts were associated with decreased IL-22 expression in bronchoalveolar lavage and were independent of hyperoxia-induced inflammasome activation. Collectively, these results demonstrate a previously unrecognized influence of the gut-lung axis during the development of neonatal lung injury, which could be leveraged to ameliorate the most severe and persistent pulmonary complication of preterm birth.

PubMed ID: 31644311 Exiting the NIEHS site

MeSH Terms: Airway Resistance/drug effects; Animals; Animals, Newborn; Anti-Bacterial Agents/adverse effects*; Bronchoalveolar Lavage Fluid; Bronchopulmonary Dysplasia/complications*; Bronchopulmonary Dysplasia/physiopathology; Cytokines/metabolism; Female; Granulocytes/metabolism; Hyperoxia/complications; Hyperoxia/physiopathology; Inflammasomes/metabolism; Leukocyte Common Antigens/metabolism; Lung Injury/chemically induced*; Lung Injury/microbiology; Lung Injury/physiopathology; Lung/pathology; Maternal Exposure*; Mice, Inbred C57BL; Oxygen/metabolism; Phenotype; Pregnancy; Prenatal Exposure Delayed Effects/pathology*; Prenatal Exposure Delayed Effects/physiopathology; Pulmonary Fibrosis/complications; Pulmonary Fibrosis/microbiology; Survival Analysis; Vascular Remodeling/drug effects

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