Microbial dysbiosis is linked to severe BPD the respiratory tract quickly becomes colonized after birth through exposure to both the mother and the environment. BPD in neonates is not only attributed to postnatal risk factors such as oxidative stress and mechanical ventilation but also to respiratory and intestinal microbial dysbiosis. Bronchopulmonary dysplasia (BPD) is a chronic lung disease that develops in premature infants due to the damage caused by hyperoxia-induced lung injury and insufficient repair mechanisms in the developing lung. Prolonged hyperoxia exposure in newborn rats reduces alveolar septation and angiogenesis, increases the terminal air gap size, and impairs lung development. However, oxygen treatment for newborns can have adverse consequences. Supplemental oxygen is frequently used to treat neonates who have respiratory problems. Respiratory distress syndrome is the most common cause of breathing difficulties in preterm newborns, affecting approximately 50% of all preterm infants born before 30 weeks of gestation. johnsonii protects against hyperoxia-induced lung injury and modulates the gut microbiota. johnsonii treatment increased the vascular density, decreased the MLI and cytokine levels, and restored the gut microbiota in hyperoxia-exposed neonatal mice. At the genus level of the gut microbiota, the O 2 + NS group exhibited significantly higher Staphylococcus and Enterobacter abundance and significantly lower Lactobacillus abundance compared with the RA + NS and RA + probiotic groups. The O 2 + NS group exhibited significantly lower body weight and vascular density and significantly higher mean linear intercept (MLI) and lung cytokine levels compared with the RA + NS and RA + probiotic groups. The right lung of each mouse was harvested for Western blot, cytokine, and histology analyses. On postnatal day 7, lung and intestinal microbiota were sampled from the left lung and lower gastrointestinal tract, respectively. We evaluated the following four study groups: RA + NS, RA + probiotic, O 2 + NS, and O 2 + probiotic. Control mice received an equal volume of normal saline (NS). johnsonii at a dose of 1 × 10 5 colony-forming units. From postnatal days 0 to 6, they were administered intranasal 10 μL L. Neonatal C57BL/6N mice were reared in either room air (RA) or hyperoxia condition (85% O 2). johnsonii on lung development in hyperoxia-exposed neonatal mice. This study investigated the protective effects of intranasal administration of L. Lactobacillus johnsonii supplementation attenuates respiratory viral infection in mice and exhibits anti-inflammatory effects. Supplemental oxygen impairs lung development in newborn infants with respiratory distress.
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