This collapse occurs in a setting of epithelial denudation, fragmentation of basal lamina, generation of inflammatory cytokines and chemotactic factors, deposition of fibrin and fibronectin, and invasion of fibroblasts into the acinus. The deposition of extracellular matrix in collapsed air spaces can cause adhesions to form between the approximated alveolar walls, preventing reexpansion after epithelial repair restores surfactant function. Thus, in experimental models of lung injury, some scars contain enormous tangles of agglomerated basal lamina when stained immunohistochemically or examined by electron microscopy (Fig 2). Gradual resorption of basal lamina may take place, for some scars contain only a few remnants of this structure.
A detailed examination of the sites of active synthesis of extracellular matrix leads to the inference that cellular contraction analogous to that of a contracting wound is also involved in lung fibrosis. Although the normal lung fibroblast has contractile features, the contractile filament bundles of fibroblasts in Masson bodies and in fibroblastic foci of UIP are exaggerated and sometimes contain dense bodies like smooth muscle cells.
Figure 2. Experimental pulmonary fibrosis in the rat induced by a single intratracheal injection of bleomycin, 7.5 units/kg, 10 days earlier. Immunoperoxidase staining for laminin shows approximated basal laminae of collapsed alveolar walls in a focus of fibrosis (X 50).