Pulmonary immune cell transcriptome changes in double-hit model of BPD induced by chorioamnionitis and postnatal hyperoxia

Preterm infants with bronchopulmonary dysplasia (BPD) have lifelong increased risk of respiratory morbidities associated with environmental pathogen exposure and underlying mechanisms are poorly understood. The resident immune cells of the lung play vital roles in host defense. However, the effect of perinatal events associated with BPD on pulmonary-specific immune cells is not well understood. We used a double-hit model of BPD induced by prenatal chorioamnionitis followed by postnatal hyperoxia, and performed global transcriptome analysis of all resident pulmonary immune cells. This is the first comprehensive report delineating transcriptomic changes in resident immune cells of the lung in a translationally relevant double-hit model of BPD.患有支气管肺发育不良（bronchopulmonary dysplasia, BPD）的早产婴儿，终生面临与环境病原体暴露相关的呼吸道疾病风险升高的问题，其潜在机制尚不明确。肺驻留免疫细胞在宿主防御中发挥关键作用。然而，与BPD相关的围产期事件对肺特异性免疫细胞的影响仍未得到充分阐明。我们采用了由产前绒毛膜羊膜炎诱导、继之以产后高氧暴露的BPD双打击模型，并对所有肺驻留免疫细胞开展了全局转录组分析。本研究是首个在具有转化研究相关性的BPD双打击模型中，阐明肺驻留免疫细胞转录组变化的综合性报告。