Further investigation is required to delineate the biochemical and cellular interactions that influence lung injury and fibrosis. The results from studies in adults, neonates, and animals suggest that fibronectin may play a key role in the development of pulmonary fibrosis following acute lung injury. Fibronectin as well as other pulmonary cytokines are essential participants in efficient and orderly wound repair; however, the excessive production of these mediators may result in an exaggeration of the normal healing process with the eventual outcome of pulmonary fibrosis. The potential role of fibronectin and other cytokines as mediators and markers of BPD may thus allow for earlier detection and identification of those infants with RDS who are at greatest risk to develop BPD, as well as aiding in the development and selection of therapeutic interventions that can more effectively treat and possibly prevent the deleterious consequences of bronchopulmonary dysplasia.