Bronchopulmonary dysplasia, or BPD, is a chronic pulmonary disorder of premature infants, commonly defined as having an oxygen requirement at 36 weeks postmenstrual age. It is an important source of morbidity and mortality in premature neonates. Its' etiology appears to be multifactorial with the most common associations being prematurity, need for mechanical ventilation, and oxygen exposure. Implied in the pathogenesis of BPD is the role of cytokines which are immune mediators produced by most cell types. This is evidenced by studies in which there exist alterations in the levels of "pro-inflammatory" and "anti-inflammatory" cytokines. The imbalance of these cytokines have either heralded the onset or predicted the presence of BPD, or indicated a decreased propensity to developing this chronic respiratory disorder of preterm infants. Many other pulmonary markers have been shown to be altered in patients with BPD. These include markers indicative of altered lung repair processes, decreased endothelial integrity, oxidative damage and abnormal fibrinolytic activity, all of which are thought to be mechanisms contributing to the development of BPD. In this review, we will discuss the physiologic role of specific biomarkers in the pulmonary tract of the human premature neonate, the perturbations that enable them to be deranged, and their proposed association with BPD.
|Original language||English (US)|
|Number of pages||13|
|State||Published - Aug 28 2008|
- Premature neonate
ASJC Scopus subject areas
- Molecular Medicine
- Biochemistry, medical