Release of Iron by Resident and Stimulated Mouse Peritoneal Macrophages following Ingestion and Degradation of Transferrin—Antitransferrin Immune Complexes

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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 Fe and degraded transferrin to the incubation medium was studied. Release of Fe 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 Fe released was in the form of ferritin. Deferrioxamine (1 mM) increased the release of Fe 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 Fe, nor did the addition of apotransferrin (1 mg/ml) to the culture medium. The concept of a blockade of Fe release by RES cells in states of inflammation is supported; it may be a primary cause of the anemia of chronic disease.