The Pathogenesis of a Laboratory Model Resembling Certain Human Interstitial Lung Diseases* by Jan R. Brentjens,~

There are increasing clinical (1-6), functional (7), radiological (4, 5, 6, 8), and histological (3, 9-14) evidences that interstitial pneumonitis with or without pulmonary fibrosis may develop in patients with underlying diseases which appear to be associated with circulating antigen-antibody complexes. The pathogenesis of these human lesions, however, has not been studied in experimental animal models. Rabbits with acute or chronic serum sickness have not shown pulmonary changes (15, 16). On the other hand, acute anaphylactic shock, a condition characterized by preferential precipitation of circulating antigen-antibody complexes within the lumina of pulmonary capillaries (17-19), is caused by a mechanism which has no relationship with chronic pulmonary diseases in man. These considerations have suggested the possibility that antigen-antibody complexes present in large amount and for prolonged periods of time in the circulation of rabbits may localize in their lungs, thereby producing inflammatory reactions comparable to those commonly seen in the kidneys of the same animals.