Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia

Abstract

Exposure to hyperoxia, invasive mechanical ventilation, and systemic/local sepsis are important antecedents of postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia (BPD). This review will summarize information obtained from animal (baboon, lamb/sheep, rat and mouse) models that pertain to the specific inflammatory agents and signaling molecules that predispose a premature infant to BPD.

Keywords: hyperoxia; infection; invasive ventilation; lung; newborn.

Figure 1. Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia (BPD)

The 3 major postnatal factors act on the immature lung initiating an inflammatory cascade involving specific cells and cytokines. Local/systemic sepsis is most prominent among the 3 to cause inflammation, followed by hyperoxia and invasive ventilation (as noted by the thickness of the arrows). These, in turn, instigate effects promoting cell death, cell cycle arrest, and abnormal production of growth factors, matrix proteins and vascular factors. Mediators that have been consistently reported to have the above noted effects have been listed in the figure. The net result is impaired alveolarization and dysregulated vascularization culminating in the pulmonary phenotype of BPD. Ang-2: Angiopoietin 2. For additional abbreviations and details, please see text.