Perinatal inflammation and lung injury

Abstract

Bronchopulmonary dysplasia (BPD) remains the major morbidity of extreme preterm birth. The incidence of BPD has remained stable despite recent efforts to reduce postnatal exposures to volutrauma and hyperoxia. This review will focus on recent clinical and experimental insights that provide support for the concept that the 'new BPD' is the result of inflammation-mediated injury and altered lung development during a window of vulnerability in genetically susceptible infants that is modified by maternal and postnatal exposures.

Figure 1

Proposed scheme of pre- and postnatal inflammation altering lung development during the vulnerable saccular stage of lung development in genetically susceptible extremely low gestational age newborns. ROS, reactive oxygen species.

Figure 2

The relationship between Ureaplasma respiratory tract colonization and duration of mechanical ventilation and risk for bronchopulmonary dysplasia (BPD). In a cohort of 230 preterm infants <33 weeks’ gestation, infants with duration of ventilation <12 days compared to infants with longer duration of mechanical ventilation were less likely to be colonized with Ureaplasma (P < 0.01) (A). Ureaplasma-colonized infants ventilated for >2 and <33 days were more likely to develop BPD than non-colonized infants (B).

Figure 2

The relationship between Ureaplasma respiratory tract colonization and duration of mechanical ventilation and risk for bronchopulmonary dysplasia (BPD). In a cohort of 230 preterm infants <33 weeks’ gestation, infants with duration of ventilation <12 days compared to infants with longer duration of mechanical ventilation were less likely to be colonized with Ureaplasma (P < 0.01) (A). Ureaplasma-colonized infants ventilated for >2 and <33 days were more likely to develop BPD than non-colonized infants (B).