Recent studies suggest that
IgA immune complex induced
lung injury in the rat is
oxygen radical mediated. A
cerium chloride (
CeCl3) method was used to ultrastructurally analyze the in situ elaboration of H2O2 in
IgA immune complex injured lungs. After induction of
IgA immune complex lung injury, the lungs were instilled with a reaction
buffer containing
CeCl3 which forms an electron-dense precipitate when exposed to H2O2. Ultrastructural examination and x-ray microanalysis revealed electron-dense
cerium deposits on the surfaces and in cytoplasmic vacuoles of alveolar macrophages located along damaged alveolar septae. Similar deposits were prominent on the
luminal surfaces of injured pneumocytes, especially alveolar type II cells. No
cerium-containing deposits were found in undamaged negative control lungs (
IgA alone without
antigen) or in lungs of rats that received
IgA immune complexes in the presence of
catalase. To further define the source of
cerium-reactive products, monolayers of rat pulmonary alveolar epithelial cells were incubated with
IgA complexes. Alveolar epithelial cells exposed to complexes produced no detectable H2O2 as measured by two spectrophotometric assays, and in the presence of
CeCl3, exhibited negligible amounts of electron-dense material regardless of the presence or absence of
catalase. The data corroborate indirect in vivo and in vitro studies which suggest that
IgA immune complex induced
lung injury is mediated by
oxygen-derived metabolites produced by lung macrophages. Use of the
CeCl3 method in intact rat lungs allows direct ultrastructural cytochemical analysis of H2O2 production in inflamed tissue.