Antenatal infection and ventilation with BPD associated with excessive accumulation of dendritic cells in lungs

Rates of premature births have increased in recent years, affecting more than 12% of all births and making strategies for managing the associated perinatal complications an important public goal. Preterm infants are particularly at risk for bronchopulmonary dysplasia (BPD), a chronic lung disease. BPD has multiple causes, and uncovering critical interactions within the immune system can lead to new approaches for treatment.

A new study reported in the January issue of the journal Pediatric and Developmental Pathology questions the role of dendritic cells in BPD. These are critical immune regulatory cells that can affect formation and development of blood vessels; however, the extent of their role in BPD has not yet been fully explained.

Very low birth-weight infants are at the greatest risk for this lung disease. Thirty percent of those born between 24 and 28 weeks of gestation are affected, and many will require long-term respiratory support. When BPD occurs, it stops alveolar development—the final branches of the respiratory tree where gas and blood are exchanged.

In the current study, postmortem lungs of preterm infants born between 23 and 29 weeks of gestational age were examined to determine the early and late effects of ventilation on both the prevalence and the distribution of dendritic cells. These patients were grouped as: (1) short-term ventilated—infants 23 to 29 weeks at time of death and ventilated for at least four days; (2) long-term ventilated—infants more than 30 weeks in total age, including at least six weeks after birth and dependent on a ventilator at least 75% of that span; (3) early control; and (4) late control. The control groups were age-matched infants who had lived less than 12 hours.

The lungs of early and late control group infants with no evidence of antenatal infection showed scattered dendritic cells in the peripheral lung tissue. In contrast, the lungs of early control infants with a history of antenatal infection and the lungs of short- and long-term ventilated preterm infants displayed a threefold increase in dendritic cells.

This study demonstrates that dendritic cells are a normal presence in the airways and tissue of more developed lungs. However, antenatal infection and ventilation with BPD are associated with excessive accumulation of dendritic cells in the lungs. This massive influx may play a part in the pathogenesis of BPD, and more clearly defining its role may lead to new therapeutic approaches to this disease.