Airway remodelling in chronic lung disease of prematurity.

Increasing numbers of very preterm survivors are developing chronic lung disease characterised by protracted respiratory insufficiency and a requirement for supplemental oxygen. An early inflammatory response results in the development of airways remodelling. Pulmonary inflammation can be triggered by any combination of antenatal infection, mechanical ventilation or oxygen toxicity and the end result is increased lung capillary permeability and leukocyte chemotaxis. The neutrophil plays a key role in initiating lung damage by releasing enzymes such as elastase and matrix metalloproteinases that disrupt the lung extracellular matrix. The extracellular matrix is essential for the normal alignment and differentiation of pneumocytes and pulmonary capillaries. This so called "new chronic lung disease" resulting from airways remodelling and arrested lung development is characterised pathologically by fewer, larger alveoli and less pulmonary fibrosis than previously described. Copyright 2002 Elsevier Science Ltd.