Bronchopulmonary Dysplasia and Inflammatory Biomarkers in the Premature Neonate

Carl L Bose ^1*, Matthew M Laughon ¹ and Christiane E L Dammann ²

¹ University of North Carolina, United States
² Tufts-New England Medical Center, United States

^* To whom correspondence should be addressed. E-mail: carl_bose{at}med.unc.edu.

Accepted 8 July 2008

Abstract

Bronchopulmonary dysplasia (BPD) is the most common, serious sequelae of premature birth. Inflammation is a major contributor to the pathogenesis of BPD. Often 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 (i.e. chemokines), proteins that facilitate the transendothelial migration of inflammatory cells from blood vessels (i.e. adhesion molecules), proteins that promote tissue damage (i.e. pro-inflammatory cytokines and proteases), and proteins that modulate the process (e.g., 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. In this manuscript, 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.