The acute respiratory distress syndrome (ARDS) is an acute and severe form of microvascular lung injury which is frequently seen in intensive therapy units. Reductions in mortality have been reported by some centres; however, 40–70% of patients still die from this syndrome.1 ,2 Treatment at present is largely supportive and, despite our increased understanding of the pathological processes involved, there are no specific treatments of proven benefit.

Interstitial and intra-alveolar fibrosis are hallmarks of the more advanced stages of ARDS and are characterised by the abnormal and excessive deposition of extracellular matrix proteins, in particular collagen.3 ,4 Histologically and biochemically this is similar to the fibrosis seen in other more chronic forms of interstitial lung disease4; however, more is known of the mediators and cellular events that occur in these disorders. The decrease in pulmonary compliance and progressive hypoxia resulting from fibrotic change leads to ventilator dependence. As a result, progressive fibrosis is a direct cause of respiratory death in up to 40% of patients3 ,5 but is also an indirect cause of death due to nosocomial infection and progressive multi-organ failure in up to 70% of patients who die from ARDS.6 Thus, the fibrotic process is an important determinant of outcome and a potential target for therapeutic intervention.