Bronchoalveolar inflammatory pathophysiology of bronchopulmonary dysplasia.

It has been emphasized that to prevent BPD ultimately, society must prevent high-risk pregnancies that result in very low birthweight infants. This represents a problem of immense magnitude that demands utmost social science attention. While attempting to solve this complex dilemma, however, RDS and BPD continue to represent the major contributors toward infant mortality and morbidity in developed nations. Certainly elucidation of the pulmonary surfactant system coupled with pharmacologic intervention to replete deficiency of this system has represented a tremendous advance in understanding and therapy of neonatal lung injury. One might make the ethical argument, however, that decreasing mortality from RDS with exogenous pulmonary surfactant mandates an equally vigorous effort toward the prevention of BPD. Elucidation of the bronchoalveolar inflammatory response that characterizes the acute aspects of BPD offers a number of novel, therapeutic approaches that are only beginning to be explored. Although exogenous steroids may indeed have a beneficial effect in reducing the incidence and severity of BPD, there are undoubtedly a number of more specific approaches relating to various aspects of pulmonary inflammation that warrant investigation. Unlike ARDS, BPD represents an ideal disease in which to conduct clinical investigations, because individuals at risk for the disease may be identified early, even before the bronchoalveolar inflammatory response is established. Accordingly, prophylactic therapeutic intervention is plausible. Potentially modulation of the pulmonary inflammatory response associated with BPD will offer clinicians an alternative to current empiric, supportive therapy for BPD; namely therapy directed at one aspect of the very molecular basis of BPD pathophysiology.