ABSTRACT
Chronic lung disease (CLD) of early infancy is a multifaceted disease that is caused by prolonged oxygen therapy or the barotrauma of assisted ventilation (1-4). Although endothelium, type II pneumonocytes, fibroblasts, and neutrophils have major roles in the pathophysiology of CLD, pulmonary macrophages are arguably the major cell type responsible for the initiation, regulation, and resolution of inflammation in this disease. The role of pulmonary macrophages is one that reaches far beyond the inflammatory responses of the immature lung to hyperoxia or physical injury. This chapter will address the pathophysiology of CLD as it relates to pulmonary macrophages. Recently reviewed subject areas include (1) the emergence of the pulmonary macrophage populations during fetal and neonatal life, (2) the role that macrophages and pulmonary infections play in the pathogenesis of chronic lung disease of early infancy, (3) the interactions of lung macrophages have with other pulmonary cells by cell-to-cell communication or mediator release, (4) the importance that macrophages have in clearing inflammatory neutrophils from the alveoli, (5) the limitations of studying lung macrophages in human neonates, and (6) future recommendations for understanding macrophages as important participants in the causation and resolution of acute
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lung injury during the neonatal period. Each topic will summarize our current knowledge related to clinical and basic research on lung macrophages of newborns, and indicate additional investigations needed to facilitate new therapeutic and preventive strategies for CLD.
