Heydarian Motaharehsadat, Schulz Christian, Stoeger Tobias, Hilgendorff Anne
Institute for Lung Health and Immunity and Comprehensive Pneumology Center with the CPC-M bioArchive, Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
German Center for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany.
Mol Cell Pediatr. 2022 Aug 2;9(1):16. doi: 10.1186/s40348-022-00148-w.
In the neonatal lung, exposure to both prenatal and early postnatal risk factors converge into the development of injury and ultimately chronic disease, also known as bronchopulmonary dysplasia (BPD). The focus of many studies has been the characteristic inflammatory responses provoked by these exposures. Here, we review the relationship between immaturity and prenatal conditions, as well as postnatal exposure to mechanical ventilation and oxygen toxicity, with the imbalance of pro- and anti-inflammatory regulatory networks. In these conditions, cytokine release, protease activity, and sustained presence of innate immune cells in the lung result in pathologic processes contributing to lung injury. We highlight the recruitment and function of myeloid innate immune cells, in particular, neutrophils and monocyte/macrophages in the BPD lung in human patients and animal models. We also discuss dissimilarities between the infant and adult immune system as a basis for the development of novel therapeutic strategies.
在新生儿肺中，产前和产后早期暴露于危险因素会共同导致肺损伤的发生，并最终引发慢性疾病，即支气管肺发育不良（BPD）。许多研究的重点是这些暴露所引发的特征性炎症反应。在此，我们综述了肺发育不成熟与产前状况之间的关系，以及产后机械通气和氧中毒暴露与促炎和抗炎调节网络失衡之间的关系。在这些情况下，细胞因子释放、蛋白酶活性以及肺中固有免疫细胞的持续存在会导致促成肺损伤的病理过程。我们着重介绍了人类患者和动物模型中BPD肺中髓系固有免疫细胞（尤其是中性粒细胞和单核细胞/巨噬细胞）的募集和功能。我们还讨论了婴儿和成人免疫系统之间的差异，以此作为开发新型治疗策略的基础。
