The destruction of type 2 pneumocytes by airborne influenza PR8-A virus; its effect on surfactant and lecithin content of the pneumonic lesions of mice.

Influenzal pneumonia has been studied in mice subjected to sublethal doses of airborne PR8-A influenza virus. Electron microscopy revealed that the virus propagated in and at the same time destroyed the ciliated and nonciliated bronchial cells and the types 1 and 2 alveolar pneumocytes. The regenerating bronchial membranes were metaplastic and grew peripherally into the surrounding alveolar ducts and alveoli to form epithelial nodules which caused obstruction and collapse of the involved lobes. The development of the lung lesions was correlated with phospholipid (lecithin) levels in consolidated and unconsolidated infected and normal lungs. As the lungs became more and more consolidated, there was a corresponding and significant decrease in the amount of phospholipid (dipalmitoyl lecithin) compared to the amount of normal or unconsolidated infected tissue. The destruction of the type 2 pneumocytes by the influenza virus and their failure to regenerate is considered to be the reason for the low phospholipid levels in the involved lobes, and thus an important cause of post-influenzal collapse in mice. The above adds additional evidence to the view that the type 2 pneumocytes are a major source of surfactant in mammalian lungs.