
This study investigated the mechanisms linking pulmonary microbial dysbiosis to worsening lung injury in bronchopulmonary dysplasia (BPD), a common lung disease in premature infants. The study found that preterm infants with Gammaproteobacteria-predominant dysbiosis have increased endotoxin in tracheal aspirates, and mice monocolonized with Escherichia coli show increased tissue damage compared to germ-free control mice. The study also developed a humanized mouse model to confirm the disease-initiating potential of airway dysbiosis. The results suggest that a lack of protective pulmonary microbiome signature attenuates an Nrf2-mediated antioxidant response, which a respiratory probiotic blend can improve, and that antioxidant pathways could be major targets for future microbiome-based therapeutics for respiratory disease.
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