Figure 4

Diagram representing inhibition of pulmonary surfactant by fibrin formation and concept of collapse induration. Under physiological conditions the phospholipid lining layer at the air–water interface reduces the surface tension and thereby promotes lung expansion upon inspiration and prevents lung collapse during expiration. In inflammatory diseases (such as ARDS, severe pneumonia) fibrinogen, leaking into the alveolus, is converted into fibrin due to a pronounced procoagulatory actvity in the alveolar compartment. Surfactant function is greatly inhibited by incorporation of hydrophobic surfactant components (PL, SP-B/C) into polymerizing fibrin. Persistence of this 'specialized' fibrin matrix promotes fibroprolifertive processes ('collapse induration'), whereas a complete lysis results in the liberation of intact surfactant material with re-opening of formerly collapsed alveoli.