Pre- and postnatal inflammatory mechanisms in chronic lung disease of preterm infants

Paediatr Respir Rev. 2004:5 Suppl A:S241-4. doi: 10.1016/s1526-0542(04)90045-0.

Abstract

Epidemiological data suggest a strong association between chorioamnionitis and the development of chronic lung disease in preterm infants. Increased concentrations of proinflammatory cytokines present in the amniotic fluid and the systemic fetal circulation seem to be important mediators in the early inflammatory response by recruiting and activating inflammatory cells and by inducing pathways of lung injury. As a consequence vascular cell adhesion molecules are upregulated and a marked infiltration of neutrophils and macrophages as well as an increased expression of interleukin-8 mRNA in the bronchoalveolar epithelium and in the interstitial tissue takes place. These antenatal events may prime the lungs such that various injurious factors in the postnatal period provoke an excessive inflammatory response: oxygen toxicity, mechanical ventilation, inappropriate resuscitation, pulmonary and systemic infections, persistent ductus arteriosus. Besides proinflammatory cytokines, toxic oxygen radicals, lipid mediators and potent proteases may be responsible for acute and chronic lung injury. In general, an imbalance between pro- and anti-inflammatory factors can be considered as a hallmark of lung injury, and may considerably affect normal alveolarisation and pulmonary vascular development by inducing growth arrest of the immature lung.

Publication types

  • Review

MeSH terms

  • Cell Adhesion Molecules / immunology
  • Chorioamnionitis / immunology
  • Chronic Disease
  • Female
  • Fetal Diseases / immunology*
  • Humans
  • Infant, Newborn
  • Infant, Premature, Diseases / immunology*
  • Inflammation / immunology
  • Inflammation Mediators / immunology
  • Lung Diseases / immunology*
  • Pregnancy

Substances

  • Cell Adhesion Molecules
  • Inflammation Mediators