Inflammation and bronchopulmonary dysplasia: a continuing story

Semin Fetal Neonatal Med. 2006 Oct;11(5):354-62. doi: 10.1016/j.siny.2006.03.004. Epub 2006 May 15.


Increasing evidence indicates that bronchopulmonary dysplasia (BPD) results, at least in part, from an imbalance between pro-inflammatory and anti-inflammatory mechanisms, with a persistent imbalance that favours pro-inflammatory mechanisms. The inflammatory response is characterised by an accumulation of neutrophils and macrophages in the airways and pulmonary tissue of preterm infants and, moreover, by an arsenal of pro-inflammatory mediators which affect the alveolar capillary unit and tissue integrity. As well as pro-inflammatory cytokines and toxic oxygen radicals, various lipid mediators as well as potent proteases may be responsible for acute lung injury. During the last decade it has become evident that multiple pre- and postnatal events contribute to the development of BPD in preterm infants. Chorioamnionitis and cytokine exposure in utero, plus sequential lung injury caused by postnatal resuscitation, oxygen toxicity, volu-, barotrauma and infection all lead to a pulmonary inflammatory response which is most probably associated with aberrant wound healing and an inhibition of alveolarisation as well as vascular development in the immature lungs of very preterm infants, causing the 'new BPD'.

Publication types

  • Review

MeSH terms

  • Bronchopulmonary Dysplasia / etiology*
  • Bronchopulmonary Dysplasia / immunology
  • Cytokines / immunology
  • Humans
  • Infant, Newborn
  • Inflammation / complications*
  • Inflammation / immunology
  • Intercellular Signaling Peptides and Proteins / physiology
  • Risk Factors


  • Cytokines
  • Intercellular Signaling Peptides and Proteins