Association of immune cell recruitment and BPD development

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.

Automated summary

Exposure to prenatal and early postnatal risk factors in the neonatal lung leads to the development of bronchopulmonary dysplasia (BPD), a chronic disease. This review focuses on the relationship between immaturity and prenatal conditions, as well as postnatal exposure to mechanical ventilation and oxygen toxicity, and the imbalance of pro- and anti-inflammatory regulatory networks. It discusses the role of myeloid innate immune cells, such as neutrophils and monocyte/macrophages, in the pathologic processes contributing to lung injury in BPD patients and animal models. The differences between the infant and adult immune system are also discussed as a basis for novel therapeutic strategies.