Fig. 1

Schematic represents the innate immune signals related to lung inflammation culminating in the BPD development and progression. Preterm infants suffer from BPD due to the impact of various risk factors including genetic background, prenatal and postnatal infections, nutrition, oxygen toxicity, and mechanical ventilation. Exposure of the structurally and functionally immature lung to these risk factors provokes oxidative stress and results in the increased expression of pro-inflammatory cytokines by resident cells in the alveolar niche. Subsequently, innate immune cells are recruited including neutrophils as the first-line defense. These events are followed by the extravasation of monocytes which eventually differentiate into macrophages in the tissue context. Neutrophil and monocyte signaling is associated with pulmonary tissue damage including impairment of epithelial and vascular function and progression of inflammatory processes. Black arrows indicate the elevating events during BPD