Effect of hypersensitivity pneumonitis on the pulmonary defense mechanisms of guinea pig lungs.

Many edemagenic and consolidating inflammatory diseases, such as virus pneumonias, of the lung are complicated by bacterial infection. Previous literature has stressed that edema and consolidation may promote bacterial proliferation by interfering with phagocytosis. To test that hypothesis, lung defense mechanisms were studied in guinea pigs with tuberculin-induced hypersensitivity pneumonitis, a noninfectious edemagenic, and consolidating inflammatory disease. Pulmonary bactericidal activity and particle clearance were measured with a mixed aerosol of (32)P-labeled Staphylococcus aureus and(35)S-labeled Proteus mirabilis. Hypersensitivity pneumonitis enhanced the bactericidal activity of the lung but had no effect on particle clearance despite the presence of consolidation and edema. These data indicate that altered host resistance to bacterial infection in acute inflammatory lung diseases can not be attributed to edema, inflammation, consolidation, changes in lung weight, etc., per se and that causes must be sought in functional changes in the bactericidal system of the lung rather than in specific histopathological changes.