Collagen and collagenase in occupational lung disease

It is apparent that the alveolar macrophage plays a central role in the pathogenesis of the fibrotic lung disorders associated with occupational exposures. While other effector cells contribute to the fibrotic process, it is the alveolar macrophage that, by virtue of its ability to expand the numbers of effector cells (i.e., neutrophils) and parenchymal cells (i.e., fibroblasts) within its local environment, can cause significant changes in the topologic organization of the alveolar structures. Through the process of neutrophil recruitment and activation, the macrophage effects major derangements to the alveolar connective tissue matrix. Furthermore, through its production of fibronectin and growth factor, the alveolar macrophage plays a central role in directing the reconstruction process by recruiting fibroblasts and expanding their numbers. In this context, fibrosis of the alveolar structures is similar to the process of scar formation following skin wounding. However, in the case of pulmonary fibrosis, the reconstruction process takes place within structures that have been so deranged by chronic inflammatory and immune processes that it is impossible to reestablish the architecture of the normal alveolar structures.