Inflammatory mediators in the immunobiology of bronchopulmonary dysplasia

Abstract

Inflammation is important in the development of bronchopulmonary dysplasia (BPD). Polymorphonuclear cells and macrophages and proinflammatory cytokines/chemokines denote early inflammation in clinical scenarios such as in utero inflammation with chorioamnionitis or initial lung injury associated with respiratory distress syndrome or ventilator-induced lung injury. The persistence and non-resolution of lung inflammation contributes greatly to BPD, including altering the lung's ability to repair, contributing to fibrosis, and inhibiting secondary septation, alveolarization, and normal vascular development. Further understanding of the role of inflammation in the pathogenesis of BPD, in particular, during the chronic inflammatory period, offers us the opportunity to develop inflammation-related prevention and treatment strategies of this disease that has long-standing consequences for very premature infants.