Release of iron by resident and stimulated mouse peritoneal macrophages following ingestion and degradation of transferrin-antitransferrin immune complexes.

Abstract

A method of loading macrophages from normal and inflammatory mouse peritoneal exudates with 59Fe using 59Fe, 125I-transferrin-antitransferrin immune complexes is described and the subsequent release of iron and degraded transferrin to the incubation medium has been studied. Release of iron occurred more rapidly from resident macrophages than from thioglycollate broth-induced (stimulated) macrophages, but degradation of the 125I-transferrin in the immune complexes was faster in stimulated cells. A small percentage of the iron released was in the form of ferritin. Desferrioxamine (1 mM) increased the release of iron from both stimulated and resident macrophages, the effect being proportionally greater in the stimulated cells. Ascorbic acid (1 mM) had no effect on the release of iron, nor did the addition of apotransferrin (1 mg/ml) to the culture medium. These results support the concept of a blockade of iron release by reticuloendothelial cells in states of inflammation, and suggest that it may be a primary cause of the anaemia of chronic disease.