PS-211 Early Postnatal Systemic Lipopolysaccharide Increases Pro-inflammatory Cytokines And Angiogenic Growth Factors In The Lungs And Leads To The Phenotype Of New Bpd In Neonatal Rats

Background Recently bronchopulmonary dysplasia (BPD) occurs not infrequently without an exposure to hyperoxia and/or mechanical ventilation in very preterm infants. To simulate the recent pattern of BPD, novel animal model of BPD induced by inflammation alone is needed. We were to establish a rat model of BPD induced by postnatal systemic lipopolysaccharide (LPS) administration alone. Methods Two days before delivery, 1 μg of LPS or vehicle (V) was injected into each amniotic sac, and after birth 0.25 mg/kg of LPS or V was injected into peritoneum of pups at P1, P3, and P5. At P7 and P14, bronchoalveolar lavage (BAL) and lung harvest were performed. BAL fluid (BALF) and peripheral blood (PB) were examined for blood cell counts and lung tissue was examined for morphometry, vascular density, neutrophil infiltration, and expressions of pro-inflammatory cytokines and angiogenic growth factors. Results Postnatal systemic LPS significantly increased the neutrophil counts in PB, BALF and within the alveoli and expressions of pro-inflammatory cytokines and angiogenic growth factors at P7. When postnatal systemic LPS was preceded by intra-amniotic LPS administration, these findings were not observed. Postnatal systemic LPS led to significant disruption of alveolar and pulmonary vascular developments at P14. Conclusions Early postnatal systemic LPS induced systemic and pulmonary pro-inflammatory responses and disrupted alveolar and pulmonary vascular developments. This rat model of new BPD induced by early postnatal inflammation per se without an exposure to hyperoxia can be used to test the effects of anti-inflammatory agents for BPD.