Abstract
Premature infants are prone to repeated lung infections after birth, which can disrupt the development of lung structure and function. However, the effects of postnatal pulmonary inflammation on lung development in newborn mice have not been reported and may play an important role in the development of bronchopulmonary dysplasia (BPD). This study aimed to establish a BPD model of postnatal pulmonary inflammation in premature infants and to explore its role and possible mechanisms in the pathogenesis of BPD. We exposed postnatal day 1 mice to lipopolysaccharide (LPS) and normal saline for 14 days. Pulmonary inflammation and alveolar microvascular development were assessed by histology. In addition, we also examined the expression of vascular endothelial growth factor (VEGF), VEGFR2, nuclear factor-kappa-B (NF-κB) and related inflammatory mediators [interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein-1α (MIP-1α), monocyte chemoattractant protein-1 (MCP-1)] in the lungs. Lung histology revealed inflammatory cell infiltration, alveolar simplification, and decreased microvascular density in LPS-exposed lungs. VEGF and VEGFR2 expression was decreased in the lungs of LPS-exposed neonatal mice. Furthermore, we detected elevated levels of the inflammatory mediators IL-1β, TNF-α, MIP-1α, and MCP-1 in the lungs, which are associated with the activation of NF-κB. Intranasal instillation of LPS inhibits lung development in newborn mice, and postnatal pulmonary inflammation may participate in the pathogenesis of BPD. The mechanism is related to the inhibition of VEGF and VEGFR2 and the upregulation of inflammatory mediators through activation of NF-κB.
Highlights
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that most often occurs in premature neonates with persistent oxygen supplementation (Davidson and Berkelhamer 2017)
The effect of inflammation on BPD has previously concentrated on intrauterine infection, but premature neonates are prone to repeated infection of the lungs due to imperfect immune system development, immature lung development, and long-term tracheal intubation or mechanical ventilation after birth (Shahzad and others 2016)
Because postnatal LPS exposure can reduce the weight of newborn mice, to further determine whether it could damage alveolar development, we evaluated the lung histology of newborn mice exposed to LPS for 14 days
Summary
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that most often occurs in premature neonates with persistent oxygen supplementation (Davidson and Berkelhamer 2017). With the development of perinatal medicine, the pathological features of BPD have changed. The etiology and pathogenesis of BPD are unknown. The effect of inflammation on BPD has previously concentrated on intrauterine infection, but premature neonates are prone to repeated infection of the lungs due to imperfect immune system development, immature lung development, and long-term tracheal intubation or mechanical ventilation after birth (Shahzad and others 2016). Postnatal pulmonary inflammation may be an important risk factor for BPD. To further investigate the possible mechanisms of BPD in postnatal lung inflammation in preterm neonates, we designed and conducted this animal experiment
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