Changes in tissue fibronectin in elastase induced lung injury.

We studied changes in rat lung fibronectin (FN) content and synthesis after endobronchial administration of elastase. A severe hemorrhagic neutrophilic alveolitis ensued with plasma protein leakage, initial rise in tissue FN content, and sustained rise in FN synthesis. Unlike fibrotic models where initial rises in tissue FN levels are sustained, levels in this model normalized promptly. This, in the setting of increased synthesis is consistent with increased degradation. This degradation of tissue FN may result in the disruption of the lung architecture, interfere with the deposition of newly synthesized matrix and could partly explain the development of emphysema in a model where excess fibronectin synthesis is observed.