Bronchopulmonary dysplasia and inflammatory biomarkers in the premature neonate

Bronchopulmonary dysplasia (BPD) is the most common, serious sequela of premature birth. Inflammation is a. or contributor to the pathogenesis of BPD. Often major initiated by a pulmonary fetal inflammatory response, lung inflammation is exacerbated by mechanical ventilation and exposure to supplemental oxygen. In response to these initiators of injury, a complex interaction occurs between proteins that attract inflammatory cells lie, chemokines), proteins that facilitate the transendothelial migration of inflammatory cells from blood vessels lie, adhesion molecules), proteins that promote tissue damage lie, pro-inflammatory cytokines and proteases), and proteins that modulate the process leg, anti-inflammatory cytokines, binding proteins and receptor antagonists). In addition, during recovery from inflammatory injury, growth factors and other substances that control normal lung growth and mediate repair influence subsequent lung structure. lit this review, we discuss the role of each aspect of the inflammatory process in the development of BPD. This discussion will include data from measurements of biomarkers in samples of fluid aspirated from the airways of human infants relevant to each phase of inflammation. Despite their limitations, these measurements provide some insight into the role of inflammation in the development of BPD and may be useful in identifying infants at risk for the disease.